SAUNDERS^ 


Tii 

intoE 


which 
cheap 
Ea 
ous  i\\\ 
most  Sn. 


nslations 


jss,  and 

;  numer- 
d  by  the 


KJ\,l  lIKlll 


ugiiipucis,  111  suiijc  cases  more  man  iM'enty  im- 
pressions being  required  to  obtain  the  desired  result.  Each  plate  is  accom- 
panied by  a  full  and  appropriate  description,  and  each  book  contains  a  con- 
densed but  adequate  outline  of  the  subject  to  which  it  is  devoted. 

One  of  the  most  valuable  features  of  these  atlases  is  that  they  offer  a 
ready  and  satisfactory  substitute  for  clinical  observation.  Such  ob- 
servation, of  course,  is  available  only  to  the  residents  in  large  medical  centers; 
and  even  then  the  requisite  variety  is  seen  only  after  long  years  of  routine 
hospital  work.  To  those  unable  to  attend  important  clinics  these  books 
will  be  absolutely  indispensable,  as  presenting  in  a  complete  and  con- 
venient form  the  most  accurate  reproductions  of  clinical  work,  interpreted 
by  the  most  competent  of  clinical  teachers. 

While  appreciating  the  value  of  such  colored  plates,  the  profession  has 
heretofore  been  practically  debarred  from  purchasing  similar  works  because 
of  their  extremely  high  price,  made  necessary  by  a  limited  sale  and  an 
enormous  expense  of  production.  Now,  however,  by  reason  of  their  pro- 
jected universal  translation  and  reproduction,  affording  international  dis- 
tribution, the  publishers  have  been  enabled  to  secure  for  these  atlases  the 
best  artistic  and  professional  talent,  to  produce  them  in  the  most 
elegant  style,  and  yet  to  offer  them  at  a  price  heretofore  unapproached 
in  cheapness.  The  great  success  of  the  undertaking  is  demonstrated 
by  the  fact  that  the  volumes  have  already  appeared  in  thirteen  different 
languages — German,  English,  French,  Italian,  Russian,  Spanish,  Dutch, 
Japanese,  Danish,  Swedish,  Roumanian,  Bohemian,  and  Hungarian. 

The  same  careful  and  competent  editorial  supervision  has  been 
secured  in  ^he  English  edition  as  in  the  originals.  The  translations  have 
been  edited  by  the  leading  American  specialists  in  the  different  sub- 
jects. The  volumes  are  of  a  uniform  and  convenient  size  (5  x  7^  inches), 
and  are  substantially  bound  in  cloth, 

(For  List  of  Books,  Prices,  etc.  see  back  cover*) 

Pamphlet  containing  specimens  of  the  Colored  Plates 

sent  free  on  application. 


UNIVERSITY  OF  CALIFORNIA 

MEDICAL  CENTER  LIBRARY 

SAN  FRANCISCO 


digitized  by  the  Internet  Archive 
in  2007  with  funding  from 
IVIicrosoft  Corporation  ~ 


http://www.archive.org/details/atlasofnervoussyOOjakorich 


ATLAS 

OF  THE 

NERVOUS  SYSTEM 

INCLUDING  AN  EPITOME  OF  THE 

Anatomy,  Pathology,  and  Treatment 


DR.  CHRISTFRIED  JAKOB 

Head  of  the  Pathologic  Institute  for  Nervous  and  Mental  Diseases  at  the 

University  of  Buenos  Ayres ;   formerly  Assistant  in 

the  Medical  Clinic,  Erlangen 


WITH    A   PREFACE   BY 


PROF.  DR.  AD.  V.  STRUMPELL 

Director  of  the  Medical  Clinic,  Erlangen 


cAuthorized  Translation  from  the  Second  Revised  German  Edition 


EDITED  BY 


EDWARD  D.  FISHER,  M.D. 

Professor  of  Diseases  of  the  Nervous  System,  University  and  Bellevue  Hospital 

Medical  College,  New  York ;  Neurologist  to  the  Department  for 

Nei-vous  Diseases,  City  Hospital,  New  York,  etc. 

With  112  Colored  Lithographic  Figures  and  139  Other  Illustrations, 
many  of  them  in  Colors 


PHILADELPHIA  AND  LONDON 

W.  B.  SAUNDERS   &    COMPANY 
1 901 


Copyright,  1901,  by  W.  B.  Saunders  &  Company 


Registered  at  Stationers'  Hall,  London,  England. 


PRESS  OF 
W.  B.  SAUNDERS   &    COMPANY 


q  /\A  ^'ol 


EDITOR'S  PREFACE. 


The  translation  of  Dr.  Jakob's  "Atlas  of  the  Nervous 
System  and  its  Diseases  "  should  prove  of  great  value  to 
the  physician.  The  book  is  virtually  divided  into  the 
Anatomy,  the  Pathology,  and  a  Description  of  the  Dis- 
eases of  the  Nervous  System. 

The  plates  illustrate  this  division  most  completely  ;  and 
especially  is  this  so  in  regard  to  the  pathology.  The 
exact  site  and  character  of  the  lesion  are  shown  in  a  way 
which  can  not  fail  to  impress  itself  on  the  memory  of  the 
reader. 

I  know  of  no  work  in  which  so  much  is  compressed 
within  so  small  a  space.  The  book  is  comprehensive  and 
practical. 

Edward  D.  Fisher. 

March,  1901. 


60^^ 


PREFACE. 


During  his  term  as  assistant  in  the  medical  clinic  of 
this  city,  Dr.  Jakob  devoted  a  great  deal  of  time  to  the 
study  of  the  normal  and  pathologic  anatomy  of  the  ner- 
vous system.  As  he  is  the  owner  of  an  extensive  col- 
lection of  histologic  sections,  prepared  by  himself  accord- 
ing to  the  best  methods  of  investigation,  he  is  in  a  position 
to  compile  the  present  atlas  for  the  most  part  from  his  own 
preparations.  I  am  sure  that  any  impartial  critic  will 
agree  with  me  that  the  illustrations  accomplish  all  that 
can  be  expected  of  illustrations.  They  present  the  actual 
conditions  in  the  plainest  and  most  intelligible  manner 
possible,  and  illustrate  very  fully  the  numerous  and  im- 
portant discoveries  which  have  been  made  in  the  study 
of  the  nervous  system.  The  student  and  the  practising 
physician  who  is  not  thoroughly  familiar  with  this  branch 
of  medical  science  can,  with  the  help  of  this  atlas,  obtain 
a  clear  idea  of  the  present  state  of  neurology  with  com- 
paratively little  trouble.  There  is  perhaps  not  another 
department  of  medicine  in  which  the  intimate  connection 
between  clinical  pathology  and  normal  and  pathologic  an- 
atomy is  so  manifest  and  so  constant  as  in  neuropathol- 
ogy. The  consistent  treatment  of  the  relations  between 
the  facts  of  normal  anatomy  and  pathology,  together  with 
the  fullness  and  attention  to  detail  shown  in  the  illustra- 
tions,— which,  although  not  schematic,  yet  give  a  compre- 
hensive view  of  the  things  they  portray, — can  not  fail  to 
be  of  the  highest  didactic  value. 

The  author  has  devoted  himself  with  untiring  industry 
to  the  task  of  achieving  a  work  of  real  and  lasting  value, 
and  I  heartily  trust  it  may  meet  with  the  success  which 
it  deserves. 

Dr.  SxRtJMPELL. 


AUTHOR'S  PREFACE. 


In  the  present  volume  I  have  endeavored  to  free  an 
important  branch  of  medicine — one  that  is  admittedly  re- 
garded by  the  majority  of  students  and  practitioners  in 
every  department  of  our  science  as  the  least  attractive, 
and  which  is,  therefore,  the  least  familiar — from  the  odium 
which  unfortunately  clings  to  it,  by  presenting  the  pecu- 
liarities of  its  normal  and  pathologic  anatomy  in  an  intel- 
ligible form. 

It  has  been  my  object  to  help  the  student  to  understand 
the  clinical  pictures  he  sees  in  the  clinics,  and  their  under- 
lying pathologic  processes,  and  to  enable  the  practising 
physician,  who  is  naturally  less  familiar  with  the  modern 
development  of  neurology,  to  grasp  the  significance  of  the 
more  important  recent  discoveries. 

I  have,  accordingly,  made  the  fullest  possible  use  of 
pictorial  representation,  and  have  kept  all  unnecessary 
details,  especially  those  relating  to  the  histology,  in  the 
background  in  the  preparation  of  the  explanatory  text. 

The  illustrations  in  the  main  present  the  actual  condi- 
tions rather  than  a  diagrammatic  version  of  them.  Al- 
though the  stained  preparations  were  found  to  be  indis- 
pensable, a  number  of  fresh,  unstained  specimens  were 
also  utilized.  It  is  to  be  remembered,  however,  that  even 
the  most  faithful  reproduction,  such  as  that  afforded  by  a 
photograph,  can  not  take  the  place  of  actual  dissection  and 
examination  of  the  fresh  brain. 

The  reproduction  of  the  specimens  in  lithographs  and 
wood-cutskwas  done  by  competent  workers  under  my  con- 
stant supervision.     The  atlas  is  founded  on  the  collection 

7 


8  A  UTHOB'S  PREFA  CE. 

of  specimens  which  I  was  able  to  gather  during  the  years 
that  I  acted  as  assistant  in  the  medical  clinic  in  Erlangcn. 

To  my  former  chief,  Dr.  von  Striimpell,  I  am  deeply 
indebted  for  his  kindness  in  placing  all  the  necessary 
material  at  my  disposition,  and  for  his  amiable  assis- 
tance in  the  elucidation  of  difficult  questions,  and  I  wish 
to  seize  this  opportunity  of  once  more  expressing  my  sin- 
cerest  thanks. 

A  word  more  in  regard  to  the  study  of  the  plates :  As 
the  space  devoted  to  the  text  was  necessarily  limited,  it 
was,  of  course,  impossible  to  give  a  minute  description  of 
tlie  wealth  of  facts  presented  for  study  by  the  illustrations, 
and  the  descriptions,  therefore,  contain  only  the  essential 
points.  I  do  not,  however,  regard  this  altogether  as  a 
disadvantage,  for  I  believe  it  will  prove  the  means  of 
supplying  the  necessary  impetus  to  careful,  independent 
study  of  the  plates,  and  thus  lead  the  student  to  form  an 
independent  opinion,  which  is  the  highest  pleasure  we  enjoy 
in  the  pursuit  of  our  science.  I  believe  the  material 
contained  in  the  plates  to  be  sufficient  for  this  purpose. 

Christfr.  Jakob. 


PREFACE  TO  THE  SECOND  EDITION. 


The  illustrations,  as  well  as  the  text  of  the  present 
edition,  have  been  carefully  revised.  The  plates  have 
been  remodeled  under  my  constant  supervision,  and  new 
ones  have  been  added,  which  have  turned  out  so  success- 
fully that  the  atlas  is  now  of  decided  value  in  scientific 
work.  The  number  of  pathologic  specimens  was  also 
increased.  The  text,  in  view  of  the  purpose  for  which  it 
is  intended,  did  not  seem  to  call  for  many  alterations ; 
some  passages  have,  however,  been  expanded,  and  the 
whole  has  been  subjected  to  a  general  revision. 

My  thanks  are  due  to  the  editor  for  his  liberality  in 
giving  me  all  the  assistance  to  make  the  volume  as  per- 
fect as  possible. 

Since  the  publication  of  the  first  edition,  translations 
into  English,  French,  Russian,  and  Italian  have  appeared, 
and  have  received  very  favorable  notices. 

Che.  Jakob. 

Buenos  Aires, 

Ospicio  de  las  Mercedes. 


LIST  OF  PLATES. 


I.  MORPHOLOGY  OF  THE  CENTRAL  NERVOUS  SYSTEM. 

PLATE 

1.  Brain  in  situ,  seen  from  above  after  removal  of  the  calvarium. 

2.  Right  hemisphere  after  removal  of  the  meninges. 

3.  Outer  surfiice  of  right  hemisphere. 

4.  Mesial  surface  of  left  hemisphere. 

5.  Base  of  the  brain. 

6.  Horizontal  section  of  the  hemispheres  immediately  above  the  corpus  cal- 

losum. 

7.  Schema  of  the  ventricular  system. 

8.  Horizontal  section  through  the  brsiin  after  the  third  ventricle  has  been 

exposed. 

9.  Horizontal  section  through  the  basal  ganglia. 

10.  Brain-stem  and  rhomboid  fossa  seen  from  above. 

11.  Four  coronal  sections  through  the  brain  of  a  dog. 

12.  Coronal  section  through  the  brain-stem  of  man. 

13.  Coronal   sections   through  the  brain-stem.     Parallel   transverse   sections 

through  the  medulla  oblongata  and  spinal  cord. 

14.  Sections  of  the  spinal  cord  in  sitn. 


II.  DEVELOPMENT  AND  STRUCTURE  OF  THE  NERVOUS 
SYSTEM. 

15.  Embryonal  area. 

16.  Development  of  the  brain. 

17.  Arrangement  of  the  neunms. 

18.  Glia  cells  and  ganglion  cells. 

19.  The  cerebral  cortex. 

20.  A  cerebral  and  a  cerebellar  convolutiim. 

21.  Cerebral  convolutions. 

22.  Motor  and  sensory  nuclei  of  cranial  nerves. 

23.  Lateral  view  of  medulla  oblongata. 

24.  Nuclei  of  the  motor  perijtheral  neurons. 

25.  Fig.  1. — Transverse  section  through  white  substance  of  spinal  cord. 
Fig.  2. — Section  through  a  spinal  ganglion. 

Fig.  3. — Cross-section  of  a  peripheral  nerve. 

26.  Figs.  1 ,  2. — Diagrammatic  representation  of  the  position  of  the  cervical 

and  lumbar  enlargements. 
Fig.  3. — The  central  canal  and  adjoining  structures. 

11 


12  LIST  OF  PLATES. 


III.  TOPOGRAPHIC  ANATOMY  OF  THE  NERVOUS  SYSTEM. 

PLATK 

27.  Distribution  of  the  cranial  and  spinal  nerves. 

2B.  Fig.  1. — Frontal  section  through  genu   of  corpus  callosuin   ami  anterior 
segment  of  frontal  lobe. 
Fig.  2. — Frontal  section  through  head  of  caudate  nucleus. 

29.  Fig.  1. — Frontal  section  through  middle  of  sej)tum  lucidum. 
Fig.  2. — Section  through  anterior  commissure. 

30.  Fig.  1. — Frontal  section  behind  anterior  commissure. 
Fig.  2. — Section  through  knee  of  inner  capsule. 

31.  Fig.  1. — Section  through  middle  of  third  ventricle. 
Fig.  2. — Section  through  central  convolutions. 

32.  Fig.  1. — Section  through  pulvinar  thalami. 
Fig.  2. — Section  through  parietal  lobe. 

33.  Fig.  1. — Section  through  occipital  lobe. 
Fig.  2. — Sagittal  section  through  brain-stem. 

Fig.  3. — Sagittal  section  through  brain -stem  and  corpus  callosura. 

34.  Fig.  1. — Horizontal  section  immediately  above  the  corpus  callosum. 
Fig.  2. — Horizontal  section  through  the  center  of  the  corpus  callosum. 
Fig.  3. — Horizontal  section  immediately  below  figure  2. 

35.  Fig.  1. — Horizontal  section  through  middle  of  optic  thalamus. 
Figs.  2,  3. — Sections  through  base  of  optic  thalamus. 

36.  Horizontal  sections  through  subthalamic  region  and  corpora  quadrigemina. 

37.  Fig.  1. — Vertical   section     through    anterior   corpora   quadrigemina  and 

pulvinar. 
Fig.  2. — Section  between  anterior  and  posterior  corpora  quatlrigemina. 

38.  Fig.  1. — Section  through  posterior  corpora  quadrigemina. 
Fig.  2. — Section  through  middle  of  pons. 

39.  Fig.  1. — Section  through  posterior  extremity  of  ]>ons. 
Fig.  2. — Section  through  nuclei  of  auditory  nerve. 

40.  Fig.  1. — Section  through  right  optic  thalamus  at  level  of  middle  commis- 

sure. 
Fig.  2. — Section  through  anterior  corpora  quadrigemina  on  left  side. 

41.  Fig.  1. — Section  through    tegmentum    behind    posterior    corpora   quad- 

rigemina. 
Fig.  2. — Section  through  nuclei  of  trigeminus. 

42.  Fig.  1. — Section  through  right   tegmental    region  at  level  of  nucleus  cf 

facial  nerve. 
Fig.  2. — Section  through  ventral  nucleus  of  auditory  nerve  on  left  side. 

43.  Fig.  1. — Section  through  cerebellum  and  medulla  oblongata. 

Fig.  2. — Section  through  medulla  oblongata  at  level  of  glossopharyngeo- 
vagus  nucleus. 

44.  Fig.  1. — Section  through  medulla  at  level  of  nuclei  of  tenth  and  twelfth 

nerves. 
Fig.  2. — Section  through  calamus  scriptorius  in  medulla. 

45.  Fig.  1. — Section  through  nuclei  in  posterior  columns. 
Fig.  2. — Section  through  medulla  below  the  olives. 

46.  Fig.  1. — Section  immediately  above  decussation  of  pyramids. 
Fig.  2. — Section  through  decussation  of  pyramids. 

47.  Fig.  1. — Section  through  spinal  cord  immediately   below   decussation  of 

pyramids. 
Fig.  2. — Section  through  spinal  cord  at  level  of  fourth  cervical  nerve. 

48.  Fig.  1. — Section  through  cervical  enlargement  at  level  of  seventh  cervical 

nerve. 


LmT  OF  PLATES.  13 


PLATE 

Figs.  2,  3. — Sections  through  thoracic  portion  of  spinal  cord. 

49.  Fig.  1. — Section  through  thoracic  portion  of  spinal  cord. 
Fig.  2. — Section  through  upper  portion  of  lumbar  cord. 
Fig.  3. — Section  through  lower  portion  of  lumbar  cord. 

50.  Fig.  1. — Section  through  middle  sacral  portion  of  cord. 
Fig.  2. — Section  through  cauda  equina  and  conuj*  meduUari-s. 

Fig.  3.— Section  through  posterior  root  and  spinal  ganglion  from  lumbar 
portion  of  cord. 

51.  Fig.  1. — Transverse  section  through  sciatic  nerve  at  its  point  of  exit. 
Fig.  2. — Longitudinal  section  of  a  nerve  bundle  from  sciatic  nerve. 
Fig.  3. — Transverse  section  of  a  nerve  bundle  from  sciatic  nerve. 
Fig.  4. — Transverse  section  of  a  normal  optic  nerve  and  sheath. 

52.  The  gray  matter  of  the  spinal  cord. 

53.  Process  of  medullation  in  the  fetal  brain. 

54.  Schema  of  the  most  important  nerve  tracts  from  a  clinical  point  of  view. 

55.  Figs.  1 ,  2. — Formation  of  tegmentum  and  crusta  from  tracts  of  cerebral 

hemispheres. 
Fig.  3. — Schema  of  optic  nerve   and   oculomotor  tract  with  their  connec- 
tions. 

56.  Fig.  1.— General  view  of  the  projection  paths. 
Fig.  2. — Schema  of  position  of  sensory  nerve  tracts. 

57.  Schema  showing  course  of  fibers  in  spinal  cord. 


IV.  GENERAL    PATHOLOGIC  ANATOMY  OF   THE    NERVOUS 
SYSTEM. 

58.  Fig.  1. — Section  through  cerebral  cortex  and  meninges  in  epidemic  cere- 
brospinal meningitis. 

Fig.  2. — Cerebral  cortex  in  tubercular  meningitis. 
69.  Fig.  1. — Aneurysm  immediately  above  corpora  quadrigemina. 

Fig.  2. — Caries  of  a  vertebra. 

Fig.  3. — Tumor  on  inner  surface  of  dura. 

60.  Fig.  1. — Brain  abscess. 

Fig.  2. — Tubercle  in  the  pons. 

61.  Fig.  1. — Chronic  hydrocephalus. 

Fig.  2. — Acute  hemorrhagic  encephalitis. 

62.  Fig.  1. — Subcortical  cerebral  focus  after  hemorrhage.     Secondary  degener- 

ation. 
Fig.  2. — Embolic  softening.     Secondary  degeneration. 

63.  A  to  F. — Products  of  degeneration  of  nerve-cells  and  fibers. 
Fig.  1. — Specimen  of  acute  myelitis. 

Fig.  2. — Specimen  of  acute  neuritis. 
Fig.  3. — Specimen  of  chronic  sclerosis. 
Fig.  4. — Specimen  of  chronic  myelitis. 

64.  Diseases  of  the  muscle-fibers. 

65.  Fig.  1. — Porencephalus,  left  hemisphere. 
Fig.  2. — Hemorrhagic  focus  in  crus  cerebri. 

66.  Fig.  1, — Section  through  anterior  corpora  quadrigemina. 

Fig.  2. — Section   through  medulla  oblongata  in  a  subject  of  hereditary 

tuberculosis. 
Fig.  3. — Chronic  progressive  ophthalmoplegia. 

gg'  \  Secondary  degenerations  of  the  crusta. 


14  LI8T  OF  PLATES. 


69.  Secondary  degenerations  of  the  pons. 

70.  Secondary  degenerations  in  the  medulla  oblongata. 

71.  Descending  degeneration  of  pyramidal  tract  in  spinal  cord  after  a  focal 

lesion  of  cerebrum. 

72.  Descending  degeneration  in  spinal  cord  in  diseases  of  the  cord. 

73.  Ascending  degeneration  of  spinal  cord. 

74.  Ascending  degeneration  in  cervical  portion  of  conl   and  medulla  oblon- 

gata. 


V.  SPECIAL  PATHOLOaY  OF  THE  SPINAL  CORD  AND  OF  THE 
PERIPHERAL  NERVES. 

75.  Various  forms  of  myelitis. 

76.  Syringomyelia. 

77.  Multiple  cerebrospinal  sclerosis. 

78.  Fig.  1. — Section  through  medulla  oblongata  in  chronic  bulbar  paralysis. 
Fig.  2. — Section  through  lower  cervical  cord  in  amyotrophic  lateral  sclerosis. 
Fig.  3. — Section  through  anterior  horn  of  cervical  cord  in  spinal  muscular 

atrophy. 

79.  Tabes  dorsalis  (thoracic  and  lumbar  portions). 

80.  Tabes  dorsalis  (cervical  region). 

81.  Spastic  spinal  paralysis. 

82.  Combined  system  diseases. 

83.  Degenerations  of  the  peripheral  nerves. 

84.  Multiple  neuritis. 


CONTENTS. 


PART  I. 

Morphology  of  the  Nervous  System. 

(Plates  1  to  14.) 

PAGE 

General  Anatomy: 

Membranes   1 

Lobes  and  convolutions  of  the  cerebral  hemispheres 3 

Interior  of  the  hemispheres.     Ventricular  system  .    6 

Optic  thalamus  and  third  ventricle 9 

Corpora  quadrigemina 12 

Cerebellum  and  fourth  ventricle 13 

Pons  and  medulla  oblongata   14 

Spinal  cord 15 

Cranial  nerves 17 

Spinal  nerves 18 

Sympathetic  system 19 

Blood-vessels.     Nerves 20 


PART  II. 

Development  and  Structure  of  the  Nervous  System.    Onto- 
genesis and  Histology  of  the  Nervous  System. 

(Plates  15  to  53.) 

The  Principal  Connecting  Fibers  : 

Development  of  the  medullary  canal 22 

Development  of  the  brain 22 

Spongioblasts  and  neuroblasts 25 

Motor  and  sensory  roots 26 

Medullation 27 

Histology  of  neuroglia,  ganglion   cells,  axis-cylinders,  and  nerve- 
fibers 27 

Neuron 28 

Commissural  fibers ^ 30 

Association  fibers 30 

Projection  fibers. ,, 32 

15 


16  CONTENTS. 


PART  III. 

Anatomy  and  Physiology  of  the  More  Important  Nervous 
Pathways. 

(Plates  64  to  57.) 

PAGE 

1.  The  Motor  Pathway: 

General  description 40 

Motor  cranial  nerves 43 

Motor  spinal  nerves 47 

2.  The  Sensory  Pathway: 

General  description 49 

Spinal  portion 51 

Cerebral  portion 53 

Sensory  cranial  nerves  and  nerves  of  special  sensation 59 

3.  The  Reflex  Paths  and  Reflex  Action 64 

4.  The  Volitional  Pathways 66 

Function  of  the  cortex.     Association  processes 67 

The  act  of  speech 69 

5.  Coordination-pathways  and  Their  Function 73 


PART  IV. 

General  Pathology  and  Treatment  of  Diseases  of  the 
Nervous  System. 

(Plates  58  to  72.) 

1.  The  causes  of  diseases  of  the  nervous  system 75 

2.  Pathologic  alterations  in  nervous  diseases 78 

3.  Symptomatology  and  topical  diagnosis  of  nervous  diseases 81 

I.  Symptoms  of  Focal  Diseases 84 

A.  Cerebral 84 

Convolutions 85 

White  matter 87 

Brain-stem  (Optic  thalamus,  corpora  quadrigemina) 88 

Pons,  medulla 89 

Cerebellum 90 

Base  of  the  brain 91 

B.  Spinal 92 

Unilateral  lesions   92 

Cervical  enlargement 93 

Thoracic  region 94 

Lumbar  enlargement 94 

Sacral  region >«......... 94 

Cauda  equina ..t.  t  «.»•«#;.  <   «*<m  ...» ^5 

C.  In  Lesions  of  the  Peripheral  Nerves ...  ^  ..,«...•..<..»«'  t .-..'.  ^  95 

Plexus  paralysis » ^  t  .•.,».»*.....«  s  k ..... .  96 

Lesions  of  the  cranial  nerves > 96 


CONTENTS.  17 

PAGE 

Lesions  of  the  more  important  spinal  nerves 100 

Disease  of  the  sympathetic    103 

II.  Symptoms  op  System  Diseases 103 

4.  General  considerations  on  methods  of  examination  and  diagnosis  , . . .  106 

History  and  general  condition  of  the  patient 106 

I.  Examination  of  the  Motor  Sphere 106 

1 .  Inspection  and  mensuration 106 

2.  Motor  irritative  symptoms 107 

3.  Motor  power 107 

4.  Power  of  coordination 108 

5.  Electrodiagnosis   108 

II.  Examination  of  the  Sensory  Sphere 113 

1.  Subjective  symptoms 113 

2.  Cutaneous  sensation  (tactile  sense,  temperature  sense,  etc.) 113 

3.  Deep  sensation 116 

4.  Special  senses 117 

Sense  of  sight 117 

Sense  of  hearing  and  of  smell    118 

Sense  of  taste 119 

III.  Examination  of  the  Reflexes 

General  remarks - 119 

Cutaneous  and  tendon  reflexes 120 

Pupillary  reflex    ... 121 

IV.  Examination  of  the  Functions  of  Bladder  and  Rectum 122 

V.   Examination  of  Trophic  and  Vasomotor  Disturbances 123 

VI.  Examination  of  the  Psychic  Functions 124 

Speech  and  writing , 124 

Memory 127 

Psychic  disturbances 128 

Diagnosis  and  prognosis 128 

5.  General  remarks  on  tho  treatment  of  nervous  diseases t  129 

Prophylaxis 130 

Curative  treatment 130 

Abstention  cures    130 

Syphilis,  malaria , 131 

Surgical  treatment    131 

Symptomatic  treatment   133 

Psychic  treatment 133 

Physical  (hygienic)   treatment 134 

Medicinal  treatment 135 


PART  V. 

Special  Pathology  and  Treatment. 

(Plates  58  to  84.) 

I.  Diseases  op  the  Membranes  and  Blood-vessels  op  the  Brain: 

1 .  Internal  hemorrhagic  pachymeningitis 136 

2.  Acute  leptomeningitis 138 

3.  Tubercular  meningitis  (PLate  68) 138 


18  CONTENTS. 


PAGE 

4.  Syphilitic  or  gummatous  meningitis  and  brain  syphilis 139 

5.  Thrombosis  of  the  sinuses 140 

6.  Diseases  of  the  arteries 141 

II.  Diseases  of  the  Brain  Substance: 

A.  Organic  Diseases  : 

Circulatory  disturbances  and  their  consequences 141 

(a)  Anemia  and  hyperemia  141 

(6)  Cerebral  hemorrhage 142 

»                (c)  Brain  embolism  and  thrombosis 145 

{d)  Aneurysm   146 

(e)  Arteriosclerosis   147 

Inflammatory  diseases  of  the  brain  substance 147 

(a)  Brain  abscess , . .  147 

(6)  Acute  encephalitis  (Plate  60).      Cerebral  paralysis  of 

children   148 

Brain -tumor  (Plate  60) 149 

Internal  hydrocephalus    151 

Paralytic  dementia    152 

Ophthalmoplegia   154 

Bulbar  paralysis    155 

Diseases  of  the  cerebellum 156 

B.  Cerebral    Diseases   of    Unknoion    Character   and   Localization 

( Cerebral  Neuroses) : 

Neurasthenia 157 

Hypochondria    158 

Hysteria 158 

Traumatic  neuroses    162 

Hemicrania  and  migraine    162 

Cephalalgia    163 

True  epilepsy 163 

Eclampsia  infantum 164 

Chorea  minor  (Sydenham's  chorea) 165 

Chronic  hereditary  chorea  (Huntingdon's  chorea) 166 

Paralysis  agitans    166 

Myotonia  congenita 166 

Idiopathic  tremor 166 

III.  Diseases  op  the  Spinal  Cord: 

A.  Diseases  Caused  by  Focal  Lesions  Livolving  a  Cross-section  of 

the  Cord : 

Diseases  of  the  spinal  meninges 167 

Hypertrophic  cervical  pachymeningitis 167 

Syphilitic  spinal  meningomyelitis 168 

Compression  myelitis  (Plate  59) 169 

Acute  and  chronic  myelitis  (Plate  75) 172 

Syringomyelia  (Plate  76) 174 

Hemorrhages  in  the  central  canal 175 

Multiple  cerebrospinal  sclerosis  (Plate  77  j 175 

B.  System  Diseases : 

Spastic  spinal  paralysis  (Plate  81) 176 

Amyotrophic  lateral  sclerosis  (Plate  78) 177 

Progressive  spinal  muscular  atrophy  (Plate  78) 177 

Neurotic  muscular  atrophy  (Plate  83) 178 

Progressive  muscular  dystrophy  (Plate  64) 179 


CONTENTS.  19 


PAGE 

Anterior  poliomyelitis  (Fig.  28) 180 

Acute 181 

Chronic 182 

Tabes  dorsalis  (Plates  79  and  80) 182 

Hereditary  ataxia 185 

IV.  Diseases  op  the  Peripheral  Nerves: 

A.  Diseases  of  Single  Nerves: 

Etiology 186 

Diseases  of  the  motor  nerves «  187 

Isolated  palsies 187 

Isolated  spasms  (occupation  neuroses) 188 

Diseases  of  the  sensory  nerves 189 

Neuralgias 190 

B.  Multiple  Neuritis 191 

Alcoholic,  diphtheric,  saturnine,  etc 192 

Infectious  multiple  neuritis  (Plate  84) 193 

Infectious  polymyositis 193 

Other  Diseases  op  the  Nervocs  System  the  Nature  and  Seat  of 
Which  are  Unknown: 

,  Basedow's  disease 194 

Myxedema 195 

Acromegaly  (Plate  83) 195 

Tetany 195 

Tetanus 196 


PART   VI. 

General  Remarks  on  Autopsy  Technic  and  the  Micro- 
scopic Examination  of  the  Nervous  System 197 


Bibliography 202 

List  of  abbreviations 203 

Index 207 


I. 

MORPHOLOGY 

OF    THK 

CENTRAL  NERVOUS  SYSTEM 

(Part  I.  of  Text.) 


Tab.l 


lith-.  Afust  /■'  Reichhold,  Mundien . 
^  .    .._. 


Tab.  1. 


PLATE  1. 

Brain  in  situ,  Seen  from  Above  after  Removal  of  the 
Calvarium. 

After  the  calvarium  has  been  removed  the  brain  is  seen 
covered  by  the  dura  mater  (left  half  of  the  plate).  The 
engorged  veins  (v)  in  the  pia- arachnoid  are  seen  through 
the  aponeurotic,  glistening  membrane,  which  appears 
tightly  stretched.  On  the  surface  of  the  dura,  lodged  in 
bony  grooves  of  the  vitreous  table,  are  the  branches  of  the 
middle  meningeal  artery,  a.  m.  (ram.  ant.,  r.  a;  ram.  post., 
r.  p).  The  superior  longitudinal  sinus  (s.  I.  s)  is  laid 
open. 

On  the  right  side  the  dura  has  been  removed  with  scis- 
sors, and  the  convolutions  on  the  convexity,  covered  by 
the  pia-arachnoid,  are  exposed.  The  veins,  which  are 
always  engorged  (especially  in  the  posterior  portions),  on 
account  of  the  position  of  the  body  before  the  autopsy, 
empty  into  the  longitudinal  sinuses.  On  either  side  of  the 
median  line  are  the  Pacchionian  bodies  (P),  consisting  of 
connective-tissue  proliferations  from  the  arachnoid,  and 
covered  with  the  arachnoidean  endothelium;  thej^  are 
often  abnormally  developed,  and  produce  marked  depres- 
sions on  the  bones  of  the  skull. 


PLATE  2. 
Right  Hemisphere  after  Removal  of  the  Meninges. 

After  the  meninges  have  been  removed  with  the  forceps 
the  convolutions  (gyri)  and  fissures  (sulci)  of  the  hemi- 
spheres are  exposed. 

Frontal  lobe:  Superior,  middle,  and  inferior  convolu- 
tions; superior  and  inferior  frontal  fissures. 

Central  convolutions :  Anterior  and  posterior  central  con- 
volutions, divided  by  the  principal  fissure,  or  sulcus  cen- 
tralis of  Rolando,  which  runs  from  above  and  behind, 
downward  and  forward.  The  junction  of  the  frontal  with 
the  anterior  central  convolution  is  called  the  foot  of  the 
convolution  (pfs,  foot  of  the  superior,  pfni,  foot  of  the 
middle,  pfi,  foot  of  the  inferior  frontal  convolution). 

Parietal  lobe:  Superior  parietal  lobule  (subject  to  many 
variations),  separated  by  the  interparietal  fissure  (ip)  from 
the  inferior  parietal  lobule,  the  anterior  segment  of  which 
is  called  the  supramarginal  gyrus,  the  posterior,  the 
angular  gyrus  (pli  courbe).  The  junction  between  the 
supramarginal  gyrus  and  the  posterior  central  convolution 
is  similarly  called  the  foot  of  the  inferior  parietal  lobule. 

Occipital  lobe :  Superior  and  middle  occipital  convolu- 
tions. 

Abbreviations. — P.  F,  frontal  pole  ;  P.  0,  occipital  pole; 
pet,  postcentral  fissure;  poc,  parieto-(M'cipital  fissure;  prci, 
inferior  precentral  fissure;  p'cs,  superior  precentral  fissure. 


Tab.  2. 


PF 


FO. 


Tnh.  •>. 


I.i'/^  "  "r/r/ihold .  Ml'.' 


^ 

Cs^ 


PLATE  3. 
Outer  Surface  of  Right  Hemisphere. 

The  convexity  of  the  hemisphere  presents,  in  addition 
to  the  lobes  described  on  plate  2,  the  temporal  lobe,  which 
is  divided  from  the  central  convolutions  and  from  the 
frontal  lobe  by  the  fissure  of  Sylvius,  The  temporal  lobe 
contains  three  convolutions — the  superior,  middle,  and 
inferior  temporal  convolutions.  The  figure  shows  also  the 
inferior  occipital  convolution. 

At  the  bottom  of  the  fissure  (or  fossa)  of  Sylvius  lies 
the  island  of  Reil,  covered  by  a  group  of  convolutions  col- 
lectively termed  the  operculum.  The  latter  is  divided  into 
the  frontal  (Op.  f),  central  (Op.  c),  and  parietal  (Op.  p) 
operculum. 

The  olfactory  bulb  is  lodged  in  a  groove  on  the  orbital 
surface  of  the  frontal  lobe. 

Abbreviations. — ip,  interparietal  fissure;  pfs,  pfm,  pfi,  foot 
of  superior,  middle,  and  inferior  frontal  convolutions;  prcs^ 
prci,  superior  and  inferior  precentral  fissure;  pet,  postcen- 
tral fissure;  sv,  ascending  limb  of  the  fissure  of  Sylvius; 
P.Fy  P.T,  P.O,  frontal,  temporal,  occipital  pole. 


PLATE  4. 
Mesial  Surface  of  the  Left  Hemisphere. 

Outer  group  of  convolutions  :  Superior  frontal  convolution, 
paracentral  lobule,  containing  the  terminal  extremity  of  the 
fissures  of  Rolando  (s.  Rol)^  precuneus  (parieto-occipital 
fissure),  cuneus  (calcarine  fissure),  lingula,  and  occipito- 
temporal convolution. 

Inner  or  marginal  group  of  convolutions :  Gyrus  fornica- 
tus,  bounded  above  by  the  callosomarginal  fissure  (f.c.m), 
gyrus  hippocampi,  and  uncus. 

Beneath  the  upper  marginal  convolution  is  the  corpus 
callosum  with  its  genu,  rostrum  (r),  and  splenium  (splen); 
under  the  corpus  callosum  the  fornix,  and  beneath  this,  the 
free  mesial  surface  of  the  optic  thalamus  (thalamus  o), 
which  i:)rojects  into  the  third  ventricle  (v.  Hi).  After  the 
septum  lucidum,  which  is  placed  anteriorly  between  the 
fornix  and  corpus  callosum,  has  been  removed,  the  cau- 
date nucleus  (n.  caud)  is  seen  on  the  floor  of  the  lateral 
ventricle. 

Abbreviations. — P.  F,  P.  0,  P.  T,  frontal,  occipital,  and 
temporal  pole;  a,  anterior  commissure;  A.  S,  aqueduct  of 
Sylvius;  c,  corpus  albicans;  Ch,  chiasm;  c.  g,  corpus 
quadrigeminum ;  g,  ganglion  habenulse;  if,  pineal  gland; 
i,  infundibulum;  is,  isthmus  of  gyrus  fornicatus;  I,  lamina 
embryonalis  ;  M,  foramen  of  Monro  ;  m,  middle  commis- 
sure; Ped,  crusta  (pes);  pla,  anterior,  pip,  posterior  fold 
of  gyrus  fornicatus;  pa,  pp,  anterior  and  posterior  con- 
necting gyri  (plicae)  between  the  gyrus  fornicatus  and  the 
precuneus;  t,  taenia  thalami;  tc,  tuber  cinereum;  teg,  teg- 
mentum; bulb,  olf,  olfactory  bulb;  tr.  o,  olfactory  tract; 
tub.  0,  olfactory  tubercle;  N,  optic  nerve;  gts,  gtm,  gti, 
superior,  middle,  and  inferior  temporal  convolutions. 


LUh.  Arost  /.'  H^AchhoM.  Afu/iOL 


Tab.  5. 


PLATE  5. 
Base  of  the  Brain. 

Frontal  lobe:  Gyrus  rectus,  a  part  of  the  superior  frontal 
convolution;  middle  frontal  convolution  (s.  tr,  triradiate 
fissure) ;  inferior  frontal  convolution. 

Temporal  lobe :  Uncus;  occipitotemporal  or  falciform  con- 
volution; inferior  temporal  convolution. 

Projecting  from  the  interior  of  both  hemispheres  the 
converging  crura  (Fed),  which  disappear  in  the  substance 
of  the  pons  (Foyis).  Below  the  pons  the  medulla  oblongata 
(i/.  obi)  with  the  pyramid  (Fy)  and  olive  (01).  Ms,  spinal 
cord. 

The  following  portions  of  the  cerebellum  are  seen:  Lobus 
sup.  med.  (Ism);  lob.  inf.  ant.  (lia),  medius  (Urn),  poste- 
rior (lip);  the  flocculus  (fl);  and  the  pyramid  of  the  infe- 
rior vermiform  process  (Fv). 

Cranial  nerves :  Olfactory  in  the  sulcus  rectus,  olfactory 
bulb,  olfactory  tract,  tuber  olfactorium.  //,  optic  nerve; 
Ch,  chiasm;  //',  optic  tract;  III,  oculomotor;  IV,  troch- 
lear; V,  trigeminus;  VI,  abducens;  VII,  facial;  VIII, 
auditory;  IX,  glossopharyngeal;  X,  vagus;  XII,  hypo- 
glossus;  and  XI,  spinal  accessory. 

Arteries:  Basilar,  vertebral,  internal  carotid  (Ca),  art. 
profunda,  art.  fossae  Sylvii  (A.f.S),  rep,  ramus  commu- 
nicans  post.;  c.a,  ramus  communicans  anterior;  c.c,  art. 
corporis  callosi. 

In  the  space  bounded  by  the  chiasm  and  converging 
crura  the  following  structures  are  seen:  Tuber  cinereum 
(t),  the  process  of  which — the  pituitary  body — has  been 
removed,  and  the  corpus  albicans  (c). 


PLATE  6. 

Horizontal  Section  of  the  Hemispheres  Immediately  above 
the  Corpus  Callosum. 

On  the  right-hand  side  the  surface  of  the  corpus  cal- 
losum is  exposed  by  a  horizontal  section.  In  front  we  see 
the  genu  (^);  behind,  the  splenium  (spl).  The  surface  of 
the  corpus  callosum  is  marked  b}^  the  longitudinal  stria?, 
or  nerves  of  Lancisi  (st.  I.  L),  by  the  rudimentary  cortical 
convolutions,  and  by  the  chordae  transversales  (Ch.  t). 

The  following  convolutions  are  included  in  the  section: 
Superior  (Jr.  .s),  middle  (/r.  med),  and  inferior  (fr.  infer) 
frontal  convolutions;  the  central  convolutions  (c.  a,  c.  p) 
with  the  fissure  of  Rolando  (s.  R)  between  them.  The 
inferior  parietal  lobule  {par.  i)  and  its  angular  gyrus 
{g.  ang);  the  middle  and  superior  occipital  convolutions 
(oc.  m,  oc.  s) ;  the  cuneus  (cun) ;  the  precuneus  (pre) ;  the 
gyrus  fornicatus  (gf);  (poc)  the  parieto-occipital  fissure. 

The  white  substance  of  the  hemisphere  (centrum  semi- 
ovale  Vieussenii)  shows  the  radiation  of  the  corpus  cal- 
losum {rad.  c.  call);  the  corona  radiata  (cor.  rad);  and  the 
cingulum  (eg). 

The  left  side  of  the  plate  shows  the  body  of  the  lateral 
ventricle  (eella  media).  In  it  we  see  the  caudate  nucleus 
(n.  caud);  stria  cornea  (str.  c);  the  lateral  segment  of  the 
optic  thalamus  (thai,  o);  the  lateral  choroid  plexus  (pi. 
ch.  I)]  and  the  fornix,  the  posterior  extremity  of  which 
disappears  in  the  descending  horn,  while  its  anterior  por- 
tion joins  the  corpus  callosum. 


Tab.  6. 


'lau. 


LUh.  Anst  F.  ReichluM.  Miincheu . 


Tab.  7. 


^F.  Reichhvid,  Mimchen . 


Tab.  7. 


Tab.?. 


"^ichhold,  Miinchen . 


Tab.  7. 


/<?d.  frontal. 


Tab.  7. 


Lith.  AnstE  Reichhxtld,  Afundien. 


Tab.  7. 


PLATE  7. 
Schema  of  the  Ventricular  System. 

The  corpus  callosum  (c.  call)  has  been  divided  through 
the  genu,  or  anterior  descending  portion,  and  through  the 
thickened  posterior  fold,  or  splenium,  exposing  in  the 
median  line  the  fornix  and  its  two  crura. 

In  front  the  interval  between  the  genu  of  the  corpus 
callosum  and  the  most  anterior  segment  of  the  fornix, 
which  is  also  reflected  downward  to  the  base  of  the  brain, 
is  filled  by  two  narrow  bands  (the  septum  lucidum)  con- 
taining between  them  the  fifth  ventricle  (v.s). 

The  section  through  the  lateral  ventricle  has  been  made  at 
a  lower  level,  so  that  the  following  structures  are  exposed : 
The  anterior  cornu  (corn,  a)  in  the  frontal  lobe,  the  poste- 
rior cornu  {corn,  p)  in  the  occipital  lobe,  and  the  descend- 
ing or  inferior  cornu  {corn,  i)  in  the  substance  of  the 
temporal  lobe,  which  is  here  assumed  to  be  transparent. 
Between  the  diverging  occipital  lobes  is  seen  the  tentorium, 
which  is  a  process  of  the  dura  mater  and  covers  the  hemi- 
spheres and  vermiform  process  of  the  cerebellum. 

The  ascending  crura  of  the  fornix  arise  in  the  descending 
cornu  at  the  free  border  of  a  thickened  fold  in  that  region, 
the  cornu  ammonis  (c.  Am),  where  they  are  known  as  the 
fimbria;  (/.  d)  fascia  dentata;  if  the  crura  are  divided  in 
front  and  the  entire  fornix  reflected  backward,  the  descend- 
ing crura  of  the  fornix  (f.d)  are  seen  descending  into  the 
substance  of  the  brain.  Beneath  the  fornix  a  delicate  vas- 
cular process  of  the  pia  mater,  the  tela  choroidea  superior, 
with  the  two  cord-like  choroid  plexuses,  is  seen.  The  cho- 
roid plexuses  pass  immediately  behind  the  descending 
crura  of  the  fornix  and  enter  the  lateral  ventricles  through 
the  foramina  of  Monro,  and  thence  pass  into  the  inferior 
cornua  as  the  plexus  choroidei  laterales. 


PLATE  8. 

Horizontal  Section  through  the  Brain  after  the  Third  Ven- 
tricle Has  Been  Exposed. 

(The  section  is  deeper  on  the  right  than  on  the  left.) 

After  the  choroid  plexuses  of  the  ascending  crura  of  the  fornix  ( / ) 
have  been  removed  and  the  cornu  ammonis  divided,  the  cavity  of  the 
third  ventricle,  bounded  on  either  side  by  the  optic  thalamus,  is 
exposed. 

On  the  left  side  is  the  free  surface  of  the  caudate  nucleus  (the  caput 
is  in  the  anterior  horn,  the  tail  extends  outward  toward  the  posterior 
horn).  The  caudate  nucleus  is  separated  from  the  optic  thalamus  by 
the  narrow  stria  cornea  {str.  c).  The  anterior  portion  of  the  optic 
thalamus  is  known  as  the  tuberculum  anticum  {t.  a),  its  posterior 
projecting  extremity  is  called  the  pulvinar  {Pul). 

In  front  of  the  descending  crura  of  the  fornix  (/.  d),  at  a  deeper 
level,  is  the  anterior  commissure;  behind  this,  in  the  middle  of  the 
third  ventricle,  the  middle  commissure  (c.  m) ;  and  in  the  posterior 
extremity  of  the  ventricle,  the  posterior  commissure  {p).  Immediately 
above  the  posterior  commissure  the  taenia  thalami  (<),  which  forms 
the  mesial  border  of  the  optic  thalamus,  unites  with  the  corresponding 
structure  of  the  other  side.  Immediately  behind  this  is  the  pineal 
gland  {E  )  (epiphysis),  flanked  by  the  ganglion  habenulae  (h).  Behind 
the  optic  thalamus  are  the  anterior  and  posterior  corpora  quadrigemina 
(qa.  qp).  Behind  the  latter  is  the  cerebellum  (C6),  which  has  been 
divided  near  the  surface,  showing  the  superior  vermiform  process  {v.  s) 
in  the  middle  and  the  hemispheres  to  either  side  (central  white  matter 
and  peripheral  cortical  gray  matter).  Isa,  Ism,  Isp,  lobus  sup.  ant., 
med.,  post.;  cd,  corpus  den tatum. 

On  the  right  side  of  the  plate  the  caput  and  tail  of  the  caudate 
nucleus  {n.  c)  are  seen  in  transverse  section.  The  convex  middle  por- 
tion has  been  removed.  We  see  also  the  optic  thalamus  in  cross-section, 
the  uppermost  layer  having  been  removed  («,  anterior,  rn,  mesial,  I, 
lateral  nucleus  of  the  optic  thalamus).  Laterally  from  the  optic 
thalamus  the  lenticular  nucleus  {n.  I),  which  with  the  caudate  nucleus 
forms  the  corpus  striatum,  makes  its  appearance.  The  area  of  white 
substance  to  the  inner  side  of  the  lenticular  nucleus  is  known  as  the 
internal  capsule  (e.  ?') ;  that  On  the  outer  side,  as  the  external  capsule 
(c.  e);  the  internal  capsule  is  divided  into  three  portions  :  The  ante- 
rior and  posterior  limbs  {cia  and  cip),  between  them  the  genu  (g),  and 
the  most  posterior  segment,  the  caps.  int.  retrolenticularis  {cirl). 

Convolutions.     (See  Plate  6.) 

Op  fr,  Op  c,  frontal  and  central  operculum  ;  ca,  anterior  horn,  ci, 
posterior  horn  of  the  ventricle  ;  c,  tail-piece  of  caudate  nucleus  ;  fli, 
inferior  longitudinal  bundle  ;  spl,  splenium  ;  s,  stria  cornea  ;  tap, 
tapetum. 


Tab.  8. 


Tah.S 


Lith.  Atisi  F.  ReidihaUi.  Munch  en . 


IVd).  .^. 


"T        .v.v-.V^' 


I.ilh.Anjil  F.  ReichhoLd,  Miinchen. 


Tab.  9. 


PLATE  9. 
Horizontal  Section  through  the  Basal  Ganglia. 

(The  level  of  the  section  is  deeper  on  the  right  than  on  the  left.) 

On  the  left  side  ( which  represents  a  deeper  level  than  the  right 
half  of  plate  8),  the  following  structures  are  seen  in  transverse  section: 
Frontal  lobe,  central  convolutions,  temporal  and  occipital  lobes;  at  the 
bottom  of  the  fissure  of  Sylvius  (/.  S)  the  convolutions  of  the  island 
of  Reil  {ins). 

The  white  matter  between  the  lenticular  nucleus  {Put)  and  the 
caudate  nucleus  {nc)  is  called  the  anterior  limb  (c.  ?'.  a),  that  between 
the  lenticular  nucleus  {gl)  and  the  optic  thalamus  the  posterior  limb 
of  the  internal  capsule  (c.  i.  p)]  the  point  where  the  two  are  joined  is 
known  as  the  knee  of  the  capsule  {g)\  its  most  posterior  segment,  as 
the  caps,  retrolenticularis  {cirl). 

Laterally  from  the  external  capsule  and  close  to  the  convolutions  of 
the  insula  is  the  claustrum  {d). 

The  lenticular  nucleus  is  divided  into  an  outer  segment — putamen 
{Put) — and  several  inner  segments — globus  pallidus  {gl). 

The  right  side  shows  a  broader  section  of  the  lenticular  nucleus;  the 
optic  thalamus  has  disappeared  and  in  its  place  we  see  the  subthalamic 
region  containing  the  red  nucleus  {n.  r)  and  subthalamic  body  [1).  The 
limbs  of  the  capsule  have  separated;  the  posterior  limb  is  now  con- 
verted into  the  crusta  or  pes  {ped).  To  the  outer  side  are  seen  the  lat- 
eral (g.  I)  and  median  {g)  geniculate  bodies. 

Embedded  in  the  white  matter  of  the  cerebellum  are  seen  the 
dentate  body  {c.  d)  and  the  tegmental  nucleus  {nt).  To  the  right  of 
the  median  line  (behind  a)  the  fourth  ventricle  appears  under  the 
vermiform  process;  the  brachium  (6r)  connects  the  region  of  the  cor- 
pora quadrigemina  with  the  cerebellum. 

Abbreviations.  — {For  the  convolutions  see  Plate  6.)  Op.fr,  Op.  c, 
Op.  p,  frontal,  central,  and  parietal  operculum;  gto,  gtm,  gti,  superior, 
middle,  and  inferior  temporal  convolutions;  got,  occipitotemporal 
convolution;  ^^rJT,  gyrus  hippocampi;  c.  ^,  cornu  ammonis;  gd,  gyms 
dentatus;  ling,  lingula;  a,  central  gray  matter  of  the  aqueduct  of 
Sylvius;  c,  tail-piece  of  caudate  nucleus;  ec,  corpus  callosum ;  ce,  ex- 
ternal capsule;  c  ex,  capsula  extrema;  E,  pineal  gland;  em,  embolus; 
/,  fornix;  fli,  inf.  long,  bundle;  fu,  fasciculus  uncinatus;  I,  lateral 
nucleus  of  optic  thalamus;  Up,  inferior  posterior  lobule ;  Isa,  Ism,  Up, 
superior  anterior,  middle,  and  posterior  lobule;  w,  mesial  nucleus  of 
optic  thalamus;  Im,  lamina  medullaris  (taenia  semicircularis) ;  ng,  nu- 
cleus globosus;  0,  optic  radiation:  ga,  corpus  quadrigeminum  anterius; 
s,  septum  lucidum;  su,  substantia  nigra;  st,  stria  (lamina)  corne-a; 
t,  taenia  thalami;  tp,  tapetum;  v,  bundle  of  Vicq  d'Azyr;  vs,  superior 
vermiform  process;  w,  Wernicke's  field. 


PLATE  10. 
Brain-stem  and  Rhomboid  Fossa  Seen  from  Above. 

The  vermiform  process  of  the  cerebellum  is  divided  by 
a  sagittal  section,  exposing  the  fourth  ventricle.  The  floor 
of  the  ventricle  is  formed  by  the  rhomboid  fossa,  which 
contains  the  ala  cinerea  (a),  calamus  scriptorius  (c),  and 
funiculi  teretes  (/.  t).  Locus  coeruleus  (Ic);  posteriorly 
on  either  side  are  the  restiform  bodies  (c.  rst)  and  the 
tuberciilum  acusticum  (ta).  At  the  entrance  of  the  aque- 
duct of  Sylvius,  covered  by  the  anterior  medullary  velum 
(v.  a),  and  frenulum  (/),  is  the  trochlear  nerve  {IV). 

In  front  of  the  rhomboid  fossa  are  the  corpora  quadri- 
gemina  anterius  (qa)  and  posterius  (qp),  and  the  median 
geniculate  body  (gm),  which  receives  the  posterior  bra- 
chium  (brp).  In  front  of  the  corpora  quadrigemina  are  the 
optic  thalami  (thai,  opt),  the  posterior  segment  of  which  has 
received  the  name  pulvinar  (Pidv),  and  between  them  the 
ganglion  habenulse  (h)  and  the  taenia  thalami  (t).  The 
pineal  gland  has  been  removed  from  its  pedicle.  Third 
ventricle  (III). 

Behind  the  rhomboid  fossa  are  the  nuclei  of  the  columns 
of  Goll  (/.  6r)  and  Burdach  (/.  B);  the  lateral  column  of 
the  spinal  cord  (/.  /);  the  nuclei  of  the  columns  of  Goll 
unite  above  to  form  the  clavae  (cl). 

Abbreviations. — In  the  vermiform  process  of  the  cere- 
bellum: Ic,  lobulus  centralis;  Ou,  culmen;  Dc,  declive;  Fc, 
folia  cacuminis;  Cb,  commissura  brevis;  Py^  pyramis;  U, 
uvula;  No,  nodulus;  Isp,  superior  posterior  lobule;  lip,  Urn, 
Ha,  inferior,  posterior,  middle,  and  anterior  lobule. 


^■pn 

^^H 

^^^^^^^^^^^^^^^^H^Hll  ^ 

^^^^^Ih 

^^^^^•^;,, 

.^^^^H 

^^^M 

^  '.^^H 

'^^^^^H 

''^^^H 

^^/■;.^J3 

l^«)iflH 

^k» 

sw^'"""^~-^B 

H^^H 

r^^Vj^^^H 

.'T~''-^"'^^^^^^^H 

^^^^^kJ^-' 

-  ^^^^^^^^^^^^^^^ 

^^^^^^H|p' 

'^i^^^^^^^^B 

^^^^^^B^ 

^^^ 

^^1 

PLATE  11. 
Four  Coronal  Sections  through  the  Brain  of  a  Dog. 

The  central  white  matter  and  the  cortex  of  the  cerebral 
hemispheres  with  its  convolutions  are  distinguished  at  the 
first  glance.  The  white  matter  is  relatively  much  smaller 
than  in  man,  and  the  convolutions  are  less  numerous. 

Fig.  1. — Section  through  the  Frontal  Lobes.  The  head  of 
the  caudate  nucleus  (n.c),  which  projects  into  the  lateral 
ventricle,  is  included  in  the  section.  The  corpus  callosum 
(c.c)  and  septum  lucidum  beneath  it  are  readily  recog- 
nized, as  well  as  the  cross-section  of  the  anterior  limb  of 
the  internal  capsule  (c.i.a).  On  the  orbital  surface  we  see 
the  optic  nerve  (//)  and  to  the  outer  side  the  olfactory 
bulb,  which  in  man  is  rudimentary. 

Fig.  2. — Section  through  the  Optic  Thalamus  (  Th. )  and  the 
Tailpiece  of  the  Caudate  Nucleus.  Beneath  the  corpus  cal- 
losum (c.c)  we  see  the  fornix  (fimbria).  Laterally  from 
the  optic  thalamus  the  internal  ^capsule, — posterior  limb 
(dp), — which  descends  to  the  pes.  (Optic  tracts,  corpora 
albicantia  (c),  descending  horn  in  the  temporal  lobe.) 

Fig.  3. — Section  through  the  Crura  Cerebri.  The  pes  (Fed) 
projects  from  the  surface  of  the  hemispheres,  which  are 
separated  from  each  other  by  the  substantia  nigra  in  the 
tegmental  region  (Z).  The  termination  of  the  optic  tract 
in  the  lateral  geniculate  body  {g.l)  and  the  pulvinar 
(Fulv)  are  seen.  The  third  ventricle  appears  beneath  the 
posterior  commissure  (cp)  and  continues  downward  as  the 
aqueduct  of  Sylvius. 

Fig.  4. — Section  through  the  Occipital  Lobes,  Cerebellum, 
and  Medulla  Oblongata.  In  the  occipital  lobe  the  posterior 
horn  of  the  lateral  ventricle  (cp),  underneath  the  vermi- 
form process  (v)  of  the  cerebellum  (Cb),  flanked  on  either 
side  by  portions  of  the  hemispheres.  The  section  of  the 
medulla  shows  the  brachia  (b),  rhomboid  fossa  (fourth 
ventricle),  tegmental  region,  pyramids  (py),  and  fibers  of 
the  pons. 


PLATE  12. 
Coronal  Section  through  the  Brain-stem  of  Man. 

(Photographs.) 

Fig.  1. — Section  through  the  Third  Ventricle  (v.m.).  We 
recognize  at  once  the  corpus  callosum  (c.c),  fornix  (/), 
lateral  ventricle  (vl),  and  caudate  nucleus  (c.  st),  and 
underneath  the  head  (tuberculum  anterius)  of  the  optic 
thalamus  (Th).  Laterally  from  this,  the  posterior  limb  of 
the  internal  capsule  (a).  Outside  and  below,  the  inner 
segments  of  the  lenticular  nucleus  constituting  the  globus 
pallidus  (gLp)  and  a  small  portion  of  the  outer  segment 
or  putamen  (Pat).  Optic  tract  (tr.o)^  corpora  albicantia 
(cm),  inferior  convolution  of  the  temporal  lobe  (uncus  of 
the  hippocampal  convolution),  nucleus  amygdalae  (n.a), 
descending  horn  of  the  lateral  ventricle,  and  gyrus  forni- 
catus  (gf). 

Fig.  2. — Section  through  the  Corpora  Albicantia,  Posterior  to 
Section  1.  Corpus  callosum  (c.c),  fornix  (/),  optic  thal- 
amus (Th),  caudate  nucleus  (c.  st),  internal  capsule  (a), 
partiall}^  emerging  at  the  base  of  the  brain  as  the  pes  (Pd), 
lateral  ventricles,  third  ventricle,  hippocampal  convolu- 
tion (g.H),  optic  tracts  (tr.  o),  substantia  nigra  (Sn),  and 
subthalamic  body  (csth). 

The  corpora  albicantia  are  coniiected  with  tlie  optic 
thalami  by  a  bundle  of  fibers,  the  bundle  of  Vicq  d'Azyr 
(v);  on  either  side  the  outer  segments  of  the  corpora  albi- 
cantia receive  the  terminations  of  the  descending  crura  of 
the  fornix  (/),  gyrus  fornicatus  (gf). 

Fig.  3. — Section  through  the  Posterior  Extremity  of  the  Third 
Ventricle,  Shortly  before  its  Conversion  into  the  Aqueduct  of 
Sylvius.  The  subthalamic  region,  situated  beneath  the 
optic  thalami  (Th),  unites  with  that  of  the  other  side; 
this  area  contains  the  red  nucleus  (nr),  lateral  white 
matter  of  the  nucleus  (Ls),  and  beneath  it  the  substantia 
nigra  (Sn).   Taenia  thalami  (t),  fasciculus  retroflexus  (/r). 

The  pes  (Pd)  projects  freely,  flanked  by  the  lateral 
geniculate  body  (gl)  with  the  beginning  of  the  optic  tract 
Itr.o). 


rig.l 


ng.S 


f^9'3. 


Tab.  12. 


LUh .  A/ust  t:  Heuliliold.  Mumhen . 


Fig.  1. 


Fig. 


Fig.  3. 


Fig.4' 


Fig.  5. 


Fig.  8.  Fig.  9.  Fig.  10. 


PLATE  13. 

Coronal  Sections  through  the  Brain=stem.     Parallel  Trans- 
verse Sections  through  the  Medulla  Oblongata 
and  Spinal  Cord. 

(Photographs.) 

Fig.  1. — Section  through  the  Anterior  Corpora  Quadrigemina.  Be- 
neath the  corpora  quadrigemina  {q.  a)  the  aqueduct  of  Sylvius  (A), 
to  either  side  the  mesial  geniculate  body  {g.  m),  and  beneath  the  latter 
the  tegmentum  (red  nucleus,  «.  r)  and  fillet  (L);  below  are  seen  the 
substantia  nigra  and  the  pes.  Beneath  the  aqueduct  lies  the  nucleus 
of  the  oculomotor  nerve. 

Fig.  2. — Section  through  the  Middle  of  the  Pons.  A  part  of  the  struc- 
tures of  the  peduncle  end  in  the  pons,  while  another  part  continues  as 
the  pyramidal  tract  {Fy)  covered  by  the  transverse  fibers  of  the  pons. 
The  brachia  (B)  leave  the  tegmentum  and  after  forming  the  lateral 
wall  of  the  fourth  ventricle,  which  is  produced  by  the  dilatation  of  the 
aqueduct  of  Sylvius,  pass  to  the  cerebellum.  The  roof  of  the  fourth 
ventricle  is  formed  by  the  vermiform  process  of  the  cerebellum  {lin- 
gula),  flanked  on  either  side  by  the  convolutions  of  the  cerebellar 
hemispheres. 

Fig.  3. — Section  though  the  Fourth  Ventricle  behind  the  Pons.  For 
the  boundaries  of  the  ventricle  see  Figure  2;  the  brachia  have  entered 
the  white  matter  of  the  cerebellum.  The  section  passes  through  the 
widest  portion  of  the  cerebellar  hemispheres  (Ob),  showing  both 
medullary  and  cortical  substance.  The  pyramids  (Py)  stand  out 
prominently,  concealing  the  structures  of  the  tegmentum  (fillet, 
nucleus  of  the  facial  nerve,  acusticus)  which  lie  on  their  dorsal  side. 

Fig.  4. — Section  Immediately  behind  the  Preceding.  The  processus 
cerebelli  ad  medullam  oblongatam  (restiform  bodies),  which  in  the 
last  section  connected  the  cerebellum  with  the  medulla,  are  now  freely 
exposed ;  in  the  white  matter  of  the  cerebellum  the  corpus  dentatum 
cerebelli  (C  d)  is  seen;  to  either  side  of  the  pyramids  {Py)  are  the 
olives.  Uvula  (J7)  of  the  vermiform  process  (  F),  nodulus  (w),  one 
of  the  cerebellar  lobes. 

Fig.  5. — Section  through  the  Posterior  Extremity  of  the  Rhomboid  Fossa 
{Calamus  Script  or  ius) .  The  restiform  bodies  approach  each  other  in  the 
median  line.     The  cerebellum  is  partially  removed. 

Fig.  6. — Section  through  the  Nuclei  of  the  Posterior  Columns  {fp), 
which  appear  in  the  Restiform  Bodies.  Py,  pyramids;  /,  beginning  of 
the  lateral  column  of  the  cord. 

Fig.  7. — Section  through  the  Decussation  of  the  Pyramids.  The  greater 
portion  of  each  pyramid  enters  the  lateral  column  of  the  opposite  side. 

Figs.  8,  9,  and  10. — Sections  through  the  Cervical,  Thoracic,  and 
Lumbar  Portions  of  the  Cord.  The  characteristic  H -shape  of  the  central 
gray  substance  is  well  shown  (anterior  horn,  posterior  horn).  The 
white  matter  is  composed  of  the  anterior,  lateral,  and  posterior  col- 
umns (/.a, /.i, /.j)). 


PLATE  14. 
Sections  of  the  Spinal  Cord  in  Situ. 

(Photographs.) 

The  white  matter  is  stained  black  in  these  preparations 
(medullary  sheatli  stain).      (See  text,  Part  VI. ) 

Fig.  1. — Cervical  Enlargement  from  a  Child,  with  Its  At- 
tachments in  the  Vertebral  Canal  (Sixth  Cervical  Vertebra  and 
Surrounding  Structures)  (Magnified  X  2) ■  The  spinal  cord  is 
surrounded  by  its  three  membranes  and  lodged  in  the  bony 
capsule.  The  anterior  half  of  the  central  gray  matter 
(anterior  horn)  sends  out  the  anterior  motor  roots  (r.a);  the 
posterior  horn,  the  posterior  sensory  roots  (r.p).  The  two 
roots  unite  and  pass  together  through  the  intervertebral  fora- 
men (f.i),  where  they  leave  the  vertebral  canal  to  enter  the 
soft  parts  as  a  peripheral  nerve  (N.p);  before  its  final 
exit  the  posterior  root  forms  the  intervertebral  or  spinal 
ganglion  (g.i)  within  the  foramen.  Body  of  vertebra 
(v),  spinous  process  (pr.  sp),  vertebral  arch  (a.v),  dura 
mater  (d). 

Fig.  2. — Lumbar  Enlargement  Surrounded  by  Its  Mem- 
branes (from,  a  New-born  Infant)  (Magnified  X  10).  The 
outer  covering  is  the  dura  mater  (dm),  which  in  the  epi- 
dural space  is  surrounded  by  Breschet's  venous  plexus 
(Pl.v)]  beneath  the  dura  mater  is  the  subdural  space;  the 
middle  envelope  is  formed  by  the  arachnoid  (ar);  the  two 
outer  envelopes  are  very  loosely  attached  to  the  cord,  but 
the  innermost,  or  pia  mater  (pm),  which  contains  the 
blood-vessels,  is  closely  adherent.  The  subarachnoid  and 
subdural  spaces  are  filled  with  cerebrospinal  fluid.  The 
anterior  (ra)  and  posterior  (rp)  roots  in  the  lumbar  en- 
largement continue  for  some  distance  within  the  vertebral 
canal  after  leaving  the  spinal  cord,  which  they  accordingly 
surround  on  all  sides;  in  deeper  sections  this  bundle  of 
nerves  forms  the  cauda  equina.  In  the  spinal  cord  we  see 
the  deep  anterior  longitudinal  fissure  (Sa);  the  shallow 
posterior  fissure;  the  anterior  (fa),  lateral  (fl),  and  poste- 
rior columns  (fp);  the  central  canal  (c.c),  which  is  the 
continuation  of  the  ventricular  system;  and  the  anterior 
and  posterior  commissures,  which  unite  the  anterior  (Ca) 
and  posterior  horns  (  Cp)  of  the  central  gray  matter. 


Tab.  14. 


i     ^M"' 


Fig.  1. 


m^jh-^. 


.J2^c^  i^mr 


II. 

DEVELOPMENT  AND  STRUCTURE 

OF    THE 

NERVOUS  SYSTEM. 

(Part  II.  of  Text.) 


Tah.lo. 


Fig.,3 


Fiff.4-. 


ihC.i 


.^  ^^^1     A 


^ 


i.t^. 


rig.  6. 

Lilh.  Anst  F.  ReirhhoUi.  Munchen . 


PLATE  15. 
Embryonal  Area. 

Fig.  1. — Section  through  the  Medullary  Groove.  The  medullary  groove 
(yellow,  m)  is  formed  from  the  ectoderm;  laterodorsally  are  the  two 
primitive  ganglionated  cords,  from  the  cells  of  which  the  intervertebral 
ganglia  are  developed.  Mesoderm,  blue;  chorda  dorsalis,  brown ;  ento- 
derm and  ectoderm,  red. 

Fig.  2. — Section  through  the  Embryonal  Area  of  a  Three-day  Chick 
Embryo.  The  medullary  canal  (m)  is  closed,  forming  in  the  middle 
the  central  canal,  to  either  side  of  which  are  the  prevertebral  plates. 
Chorda  dorsalis  (c^),  on  either  side  the  primitive  blood-vessels  (?;), 
urinary  tracts,  etc. 

Fig.  3. — Section  through  the  Medullary  Canal  {First  Month).  The 
stratified  epithelial  cells  which  compose  the  wall  are  differentiated  into 
spongioblasts  (supporting  substance)  and  neuroblasts  (nervous  sub- 
stance). On  the  ventral  side  (v)  the  anterior  roots  {ra)  are  beginning 
to  grow  from  the  neuroblasts,  which  form  the  primitive  anterior  horns; 
on  the  dorsal  aspect  the  sensory  posterior  roots  (r.p)  pass  out  from  the 
cells  of  the  spinal  ganglia  {g.i)  into  the  two  dorsal  segments  of  the 
spinal  cord. 

Fig.  4. — Section  through  the  Spinal  Cord  from  the  Second  Month.  The 
central  gray  matter  is  better  supplied  with  nuclei  and  is  beginning 
to  be  differentiated  from  the  peripheral  white  substance;  the  anterior 
(m)  and  posterior  (cp)  horns  are  formed;  roots  as  in  figure  3;  central 
canal  (c). 

Fig.  f). — Section  through  the  Spinal  Cord  from  the  Eighth  Jfonth.  In 
the  white  substance  the  various  systems  of  nerve-fibers  successively 
undergo  the  process  of  medullation,  so  that  nerve  tracts  anatomically 
and  functionally  related  reach  their  full  development  at  the  same 
time.  The  pyramidal  tract  {Py. I  and  a)  and  certain  portions  of  the 
posterior  columns  (g)  are  the  last  to  become  medullated.  The  details 
of  the  process  can  be  studied  in  the  figure,  as  the  fibers  already  covered 
with  the  medullary  sheath  are  stained  black,  while  the  nonmedul- 
lated  portions  are  unstained  and  appear  brownish  in  color. 

Fig.  6.  —Medulla  Oblongata  of  a  Six-weeks  Embryo.  Lamina  funda- 
mentalis  (//);  lamina  ependj'mica  (/e);  lamina  tegmenti  {It);  VIII, 
XII,  acusticus,  hypoglossus;  Fy,  pyramids;  v.  IV,  fourth  ventricle. 


PLATE  16. 
Development  of  the  Brain. 

Fig.  1. — Brain  and  Cord  from  the  Third  Month.  The 
forebrain  (/)  is  already  divided  into  its  hemispheres,  and 
covers  the  interb rain  and  midbrain  (///)  (primitive  optic 
thalami  and  corpora  quadrigemina).  Posteriorly  the  hind- 
brain  (IV)  (primitive  cerebellmn)  and  afterbrain  ( F) 
(primitive  medulla).  The  cord  shows  the  position  of  the 
two  enlargements  (J.  Cand  J.L). 

Fig.  2. — Base  of  the  Br  am  {Fourth  Month).  The  frontal 
lobe  is  divided  from  the  temporal  lobe  (/>./.,  Lt)  by  the 
fissure  of  Sylvius  (F.S);  the  chiasm  (11)  and  the  pes  (Pe) 
are  distinguishable.  Cerebellum  (C.b),  pyramids  (,Py), 
olives  (o). 

Fig.  3. — Mesial  Surface  of  the  Brain  (^Fourth  Month). 
The  corpus  callosum  (c.c)  and  fornix  (/)  are  readily  recog- 
nized; in  front  and  between  the  two  is  the  septum  lucidum 
(s.p).  The  descending  limb  of  tlie  fornix  is  reflected 
downw^ard  and  backward  and  ends  in  the  corpus  albicans. 

Fig.  4. — Outer  Surface  of  the  Cerebral  Hemispheres  (Sixth 
Month).  The  upper  surface  shows  a  few  fissures.  The  fis- 
sure of  Rolando  grows  from  above  downward,  the  fissure 
of  Sylvius  (fS)  from  below  upward.  At  the  bottom  of 
the  fissure  of  Sylvius  the  primitive  island  (/).  Cb,  cere- 
bellum; P,  pons;  Py,  pyramid;  o,  olive;  Mo,  medulla  ob- 
longata. 

Fig.  5. — Me-nal  Section  through  the  Primitive  Brain  of  a 
Two  and  One-half  Months^  Embryo.  The  roofoi  the  primitive 
ventricular  cavity  is  formed  by:  Lamina  tegmenti  (It); 
cerebellum  (Cb);  primitive  corpora  quadrigemina  (qp,  qa); 
epiphysis  (E);  taenia  thalami  (t  th) ;  pallium  of  the  cerebral 
vesicle  (I).  The  floor  is  formed  by  the  bulb  of  the  me- 
dulla (Mo);  pons  (P);  corpus  albicans  (c);  hypophysis 
(H);  and  in  front  of  the  latter,  the  lamina  embryonalis. 
The  optic  thalamus  (Th),  foramen  of  Monro,  subthalamic 
region,  and  olfactory  bulb  are  shown. 


Tab.  16. 


Fig.l. 


'^^f^ 


) 


Fuj.^. 


Liih.  AriMt  F.  Eeichhald.  Miinchcn. 


Tab.l7. 


Eig.S 


FigJ. 


lUh.  Anst  E  ReicMwld,  Miinnhen . 


PLATE  17. 
Arrangement  of  the  Neurons. 

Each  neuron  consists  of  a  nerve-vessel  and  its  process, 
the  nerve-fiber;  the  cells,  as  well  as  the  fiber,  give  off 
numerous  protoplasmic  processes.  We  distinguish  neurons 
with  long  and  with  short  nerve  processes  (Deiters'  and 
Golgi's  types). 

Fig.  1. — A  Pyramidal  Cell  from  the  Cortex  of  the  Cere- 
brum, with  its  Dendritic  Ramifications  (Dendrites,  Proto- 
plasmic Processes).  Each  process  gives  off  a  great  number 
of  bud-like  branches.  The  nerve-fiber  of  the  cell,  or  axis- 
cylinder  process,  is  designated  ax.  The  terminal  fibrils 
of  the  axis-cylinder  i)rocess  are  situated  at  some  distance 
from  the  cerebral  cortex  in  other  portions  of  the  brain  or 
cord,  where  they  surround  the  dendrites  of  a  ganglion 
cell.  (Fig.  2.)  This  neuron  begins  and  ends  within  the 
central  organ,  and  is,  therefore,  termed  a  central  neuron. 

Figure  2  shows  a  ganglion-cell  with  its  dendrites  from  the 
anterior  horn  of  the  spinal  cord  ;  among  its  ramifications 
are  seen  the  terminal  fibrils  of  the  nerve-fiber  belonging  to 
the  central  neuron.  The  axis-cylinder  process  (ax)  emerges 
from  the  central  organ  and  passes  to  the  soft  parts  in  the 
periphery.  The  entire  neuron  is,  therefore,  called  a  per- 
ipheral neuron. 

Figure  3  shows  diagrammatically  the  manner  in  which 
these  neurons  unite  to  form  the  nervous  pathway,  espe- 
cially the  motor  or  corticomuscular.  The  terminal  fibrils 
of  the  (red)  central  niotor  neuron  (?7io)  surround  the  cell 
of  the  (blue)  peripheral  neuron  (mp).  The  sensory  path- 
way is  built  up  in  a  similar  manner  from  three  or  more 
neurons.  The  (brown)  peripheral  sensory  neuron  termi- 
nates with  its  terminal  fi))rils  around  the  cell  of  the  (green) 
central  sensory  neuron.  The  arrangement  of  the  terminal 
fibrils  in  the  centrifugal  motor  neurons  is  the  exact  oppo- 
site of  that  which  obtains  in  the  sensory  centripetal  neu- 
rons. These  colored  pathways  are  known  as  projection 
pathways.  Within  the  cortex  certain  other  .neurons,  col- 
ored black,  indicate  the  numerous  connections  between  the 
different  parts  of  the  cortex.  They  are  known  as  the  asso- 
ciation paths  and  commissural  paths.  (For  further  descrip- 
tion the  reader  is  referred  to  the  text,  Part  III. ) 


PLATE  18. 
Qlia  Cells  and  Ganglion  Cells. 

Figs.  a-d. — Glia  Cells  from  the  White  Matter,  a  ;  Gray 
Matter  of  the  Cerebrum,  b ;  c  and  d,  from  the  Cortex  of  the 
Cerebellum.     These  cells  are  called  astrocytes  (silver  stain). 

Figs,  e  and  f. — Ganglion  Cells  Stained  with  Silver:  e, 
From  the  optic  thalamus;  /,  from  the  cerebellar  cortex  (cells 
of  Parkinje);  showing  numerous  ramifications. 

Fig.  g. — Neuroblasts  with  Primitive  Nerve-fibers,  from  the 
Anterior  Horn  of  a  Fetus. 

Figs.  1  and  2. — Motor  ganglion  cells  from  the  anterior 
horn  of  the  spinal  cord,  stained  with  methylene-blue, 
showing  their  characteristic  granulation,  nucleus,  and 
nucleolus.     In  some  places  there  is  marked  pigmentation. 

Figs.  3  and  4. — Pyramidal  Cell  from  the  Cerebral  Cortex 
Stained  loith  Methylene-blue. 


TabAS, 


Lull.  Atist  /'.'  Reu'/ihold .  Miincheu . 


Tab.  19. 


Liffi.  Anst  F.  Reichhold.  Miinrhen 


PLATE  19. 
The  Cerebral  Cortex. 

The  left  side  of  the  figure  shows  the  arraiigenjeiit  of  the 
cells  (the  outer  portions  are  stained  with  silver,  the  center 
with  methylene-blue) ;  the  right  side  shows  the  arrange- 
ment of  the  fibers;  the  two  portions  are,  of  course,  ana- 
tomically related. 

The  cells  of  the  cortex  may  be  divided  into  six  la3'ers: 
(1)  Stratum  zonale,  containing  small  polymorphous  cells 
of  the  Golgi  type;  (2)  the  first  layer  of  small  pyramidal 
cells;  (3)  the  layer  of  medium-sized  and  large  pyramidal 
cells;  (4)  the  second  layer  of  closely  packed  small  pyr- 
amidal cells;  (5)  the  second  layer  of  medium-sized  and 
large  pyramidal  cells  with  a  few  giant  pyramidal  cells;  (6) 
the  lowest  layer  of  polymorphous  cells  lying  partly  within 
the  white  substance. 

The  nerve-fibers  of  the  cortex  for  the  most  part  pass 
from  the  cerebral  medulla  into  the  cortex;  collected  into 
bundles  they  enter  the  second  layer  of  cells,  where  their 
terminal  fibrils  end;  these  radial  bundles  (radii)  therefore 
have  a  vertical  arrangement.  They  are  crossed  at  right 
angles  by  other  fibers  running  parallel  with  the  surface  of 
the  cortex  and  forming  the  so-called  plexus  of  tangential 
fibers — the  superradial  reticulum  above  the  radii,  and  the 
interradial  reticulum  within  the  radii.  The  six  layers  are 
arranged  as  follows:  (1)  The  stratum  zonale,  containing 
the  most  superficial  layer  of  tangential  fibers  immediately 
under  the  pia  mater;  (2)  the  superradial  reticulum,  in  the 
free  upper  border  of  which  there  is  a  robust  layer  of  fine 
tangential  fibers  known  as  Bechterew-Kaes'  stripe;  this 
layer  is  composed  entirely  of  very  delicate  transverse  fibers, 
and  contains  the  terminal  fibrils  of  the  radial  bundles; 
(3)  a  dense  collection  of  coarser  tangential  fibers  ( Bail- 
larger' s,  Gennari's.  Vicq  d'Azyr's  stripes,  the  latter  being 
best  developed  in  the  cortex  of  the  cuneus);  (4)  the  inter- 
radial reticulum  of  tangential  fibers;  (5)  the  layer  of 
closely  packed  radial  bundles  containing  a  few  transverse 
fibers;  (6)  the  medullar}^  layer,  containing  the  radiating 
white  fibers  (projection,  commissural,  and  long  association 
tracts)  and  the  transverse  short  association  bundles  (Mey- 
nert's  arcuate  fibers). 


PLATE  20. 
A  Cerebral  and  a  Cerebellar  Convolution. 

Fig.  1. — Cerebral  Convolution  from  the  Center  of  the  Ante- 
rior Central  Convolution  (carmin  medullary  sheath  stain). 
The  white  matter  is  stained  blue-black;  the  radial  bundles 
(r)  radiate  in  all  directions  and  end  in  the  cortex.  Pass- 
ing from  without  inward,  we  distinguish  the  following 
layers  :  The  outermost  subpial  layer  (a);  the  zonal  layer 
(^);  the  layer  of  pyramidal  cells,  which  also  present  a 
radiating  arrangement  and  contain  Baillarger's  stripe;  the 
radiation  of  projection  fibers  (r),  containing  the  outer  and 
inner  association  layer  (Meynert's  arcuate  fibers,  M);  and 
finally  the  dense  network  of  white  matter  {F). 

Fig.  2. — Cerebellar  Convolution  (Silver  Stain).  From  the 
narrow  medullary  substance,  which  is  stained  black,  a  few 
isolated  fibers  are  seen  passing  through  the  granule  layer 
(yellowish-brown)  to  the  cortical  layer  proper,  which  is 
stained  yellow  and  is  also  very  narrow.  At  the  base  of 
the  cortical  layer  we  see  a  row  of  cells  of  Purkinje,  with 
their  elaborate  arborizations.  (See  Plate  18.)  A  few 
moss-like  fibers  (r)  are  shown  in  the  cortex,  and  some 
individual  granule  cells  at  g. 


0^ 


;-':s.8i 


s^-«Sl»^ 


PLATE  21. 
Cerebral  Convolutions. 

Figures  1  and  2  show  diagrammatically  the  convolutions  and 
fissures  of  the  cortex  on  the  outer  and  mesial  surfaces  of  the  cerebral 
hemispheres.  In  the  frontal  lobe  we  recognize  three  convolutions  {g. 
.mp.,  med.,  inf ) ;  behind  this,  separated  by  the  sulcus  centralis,  the  tvfo 
central  convolutions  {g.  centr.  ant  and  2)ost),  which  merge  in  the 
median  line  into  the  paracentral  lobule;  the  parietal  lobe  contains  an 
upper  and  a  lower  group  of  convolutions,  the  lower  being  divided  into 
the  supramarginal  convolution  and  angular  gyrus  (pli  courbe),  while 
the  upper  is  continuous  on  the  mesial  surface  with  the  precuneus.  In 
the  occipital  lobe  we  distinguish  three  convolutions  {snp,  mcd,  inf); 
on  the  mesial  surface  the  lobe  is  represented  by  the  cuneus  and  lingula, 
separated  by  the  calcarine  fissure.  The  temporal  lobe  contains  three 
convolutions  {gyr.  sup,  med,  inf);  on  the  mesial  surface  the  occipito- 
temporal convolution  is  continuous  with  the  lower  marginal  convolu- 
tion (known  as  the  hippocampal  convolution ),  the  anterior  portion  of 
which  is  called  the  uncus.  The  upper  marginal  convolution  corre- 
sponds to  the  gyrus  fornicatus. 

Fig.  3. — The  Position  of  the  Psychomotor  and  Psychosensory  Cortical 
Centers  in  the  Cavity  of  the  Skull.  The  cerebral  cortex  contains  the 
motor  and  sensory  centers  for  the  periphery  of  the  body.  The  centers 
which  are  definitely  known  are  situated  in  the  central  convolutions,  in 
the  paracentral  lobule  at  the  base  of  the  three  frontal  convolutions,  in  the 
superior  temporal  convolution,  and  in  the  cortex  of  the  occipital  lobe, 
especially  on  the  mesial  surface.  The  distribution  and  the  boundaries 
of  the  various  centers  are  clearly  shown  in  the  figure:  BC,  motor  cen- 
ter for  the  lower,  AC,  for  the  upper,  extremities;  VII  C,  center  for 
the  muscles  innervated  by  the  facial ;  XII  C,  for  those  innervated  by 
the hypoglossus nerves;  31  Sp  C,  motor,  S  Sp  0,  sensory,  speech-center; 
S  C,  visual  center  (especially  on  the  mesial  surface,  cuneus);  S s,  sen- 
sory sphere  (trigeminus,  extremities).  In  front  of  BC  is  the  center  for 
the  movements  of  the  trunk;  in  front  oi  AC  the  center  for  movements 
of  the  head  and  eyes  (?),  at  the  base  of  the  upper  and  middle  frontal 
convolution.  The  order  in  BC  and  J  C  from  above  and  in  front  down- 
ward and  backward  is  as  follows:  hip,  knee,  foot  (for  BC);  shoulder, 
elbow,  hand  ( for  ^  T ) .  ( Consult  also  Part  IV. )  The  upper  extremity 
of  the  central  fissure  is  situated  5  cm.  behind  the  coronal  suture.  A 
sagittal  section  through  the  root  of  the  nose  and  the  external  occipital 
protuberance  passes  a  little  below  the  posterior  limb  of  the  fissure  of 
Sylvius.  The  central  fissure  forms  an  angle  of  about  67  degrees  with 
this  line.  If  we  divide  this  so-called  Rolando's  line  into  three  parts, 
we  have  approximately  the  positions  of  the  motor  centers  (leg,  arm, 
face). 


Tab.  2 1 


Fig.3, 


IMh.  Anat.  K  Heichtudd.  Miincheu 


PLATE  22. 

Figure  1  shows  the  position  of  the  motor  and  sensory- 
nuclei  in  which  the  cranial  nerves  originate  or  terminate. 
Their  relative  positions  are  indicated  in  the  figure,  which 
shows  the  brain-stem  and  medulla  oblongata  as  seen  from 
above. 

The  motor  cranial  nerves  originate  in  the  blue  nuclei; 
the  sensory  end* in  the  green  nuclei.  The  cells  of  the  green 
nuclei  form  the  beginning  of  the  sensory  neuron.  (See 
Plate  17.)  The  Roman  numbers  refer  to  the  cranial 
nerves.  (V  n,  nasal  descending  motor,  Fc,  caudal  de- 
scending sensory  root  of  the  trigeminus;  Vm,  motor,  V  s, 
sensory  nucleus  of  the  trigeminus;  VIII  c  Ny  cochlear; 
VIII V  iV,  vestibular  nerves. ) 

'Fig.  2. — a  to /show  various  isolated  nerve-fibers,  which 
together  make  up  the  white  substance  of  the  brain,  the 
columns  of  the  cord,  and  the  peripheral  nerves,  and  are 
not  altogether  wanting  in  the  gray  substance.  Each  nerve- 
fiber  contains  as  its  principal  constituent  the  axis-cylinder, 
which  is  surrounded  by  a  medullary  sheath  of  variable 
thickness,  the  white  medullary  sheath,  divided  into  segments 
by  the  nodes  of  Ranvier.  The  peripheral  nerves  are  pro- 
vided with  an  additional  layer  of  extreme  tenuity,  the 
sheath  of  Schwann,  situated  within  the  medullary  sheath. 

(a)  Medullated  nerve-fibers  in  longitudinal  section. 
The  medullary  substance  is  stained  black  and  obscures  the 
axis-cylinder,  which  is  better  seen  in  the  transverse  sec- 
tion (6);  (c)  a  node  of  Ranvier;  d  and  /,  transverse  and 
longitudinal  sections  stained  with  nigrosin ;  e,  isolated  fibers 
in  the  recent  state,  swollen  from  immersion  in  salt  solu- 
tion. 

The  axis-cylinder  is  composed  of  a  large  number  of 
single  so-called  ultimate  fibrillae. 


Tab.  22. 


Iig.l 


^ 


d) 


V 
lith.  Anst.  F.  Reichhnld  Miuicher, 


^ 


PLATE  23. 

Lateral  View  of  the  Medulla  Oblongata,  showing,  in  Sche- 
matic  Form,  the  Positions  of  the  Nuclei  and  the  Course 
of  the  iCranial  Nerves  within  the  white  Substance. 

The  highest  nerve  is  the  oculomotor  (III),  the  nucleus  of  which  is 
divided  into  several  jxjrtions  and  occupies  an  area  of  considerable  ex- 
tent in  the  central  gray  matter  underneath  the  aqueduct  of  Sylvius. 
Posteriorly  is  the  nucleus  of  the  trochlear  nerve  {IV)  ;  it  is  the  only 
cranial  nerve  which  emerges  on  the  dorsal  surface  of  the  brain,  where 
it  makes  its  appearance  behind  the  posterior  corpora  quadrigemina 
and,  after  crossing  that  of  the  other  side,  passes  to  the  base  of  the  brain. 

The  trigeminus  ( V)  originally  consists  of  two  distinct  parts  :  The 
anterior  motor  portion  {Vm)  springs  from  the  motor  nucleus  of  the 
fifth  nerve,  and  is  probably  joined  by  the  motor  nasal  descending  root 
{radix  superior),  which  arises  laterally  from  the  aqueduct.  The  pos- 
terior sensory  portion  (  F.s)  springs  from  the  Gasserian  ganglion,  and 
subdivides  into  three  portions  in  the  pons  :  one  x)ortion  ends  in  the 
sensory  nucleus  of  F,  another  passes  as  the  caudal  descending  root 
{radix  inferior)  through  the  medulla  oblongata  to  the  upper  portion  of 
the  cervical  enlargement,  and  is  gradually  lost  in  this  region;  a  third 
portion  goes  to  the  cerebellum.  The  facial  nerve  (  VII)  arises  from  its 
long  nucleus,  which  is  deeply  seated.  In  the  medulla  the  fibers  collect 
and  rise  toward  the  surface  to  form  the  knee  of  the  facial,  which  sur- 
rounds the  nucleus  of  the  abducens  {^^I )  and  passes  first  outward  and 
finally  downward  to  its  point  of  exit  at  the  base  of  the  brain.  The 
course  of  the  abducens  is  very  simple.  The  auditory  nerve  ( VIII) 
ends  as  the  cochlear  nerve  (  VIII  e)  in  the  ventral,  and  as  the  vestibular 
nerve  {VII  v)  in  the  dorsal  nucleus  of  the  auditory  nerve  and  its 
immediate  neighborhood.  One  portion  continues  for  some  distance 
caudad  as  the  descending  root  of  VIII.  The  sensory  fibers  of  the 
glossopharyngeal  and  vagus  arise  in  the  jugular  and  petrosal  ganglia, 
and  end  in  the  sensory  nuclei  of  IX  in  the  posterior  extremity  of  the 
floor  of  the  fourth  ventricle  (X,  green);  one  portion  continues  for  some 
distance  caudad  as  the  descending  root  of  X  {fasciculus  solitarius ) .  The 
motor  fibers  arise  in  part  from  the  nucleus  ambiguus  (X,  blue),  in  part 
from  the  nucleus  of  the  spinal  accessory. 

The  nucleus  of  the  hypoglossus  {XII),  which  is  situated  in  the 
caudal  dorsal  segment  of  the  medulla,  sends  its  fibers  through  the  sub- 
stance of  the  medulla,  on  the  surface  of  wl^ich  they  emerge  laterally 
from  the  pyramids.  The  nuclei  of  the  spinal  accessory  {XI)  extend 
far  down  into  the  upper  portion  of  the  cervical  enlargement.  The 
fibers  emerge  on  the  surface  of  the  lateral  columns;  r.  p,  highest  pos- 
terior cervical  roots  from  the  spinal  ganglia;  r.  a,  highest  anterior  roots 
of  the  cervical  enlargement. 


PLATE  24. 

Nuclei  of  the  Motor  Peripheral  Neurons  (carmin  medullary 
sheath  stain). 

Figure  1  shows  a  segment  of  the  gray  anterior  horn, 
with  its  motor  ganglion  cells,  from  the  cervical  enlarge- 
ment. The  cells  give  origin  to  the  anterior  spinal  roots 
(a.  r),  which  pass  through  the  adjoining  white  substance 
of  the  anterolateral  tracts  (black  mednllated  fibers  seen  in 
transverse  section).  The  fine  mednllated  fibers  which 
surround  the  cells  are  in  part  concerned  in  the  transmission 
of  reflexes  (reflex  collaterals  from  the  posterior  roots). 

Figure  2  represents  a  portion  of  the  nucleus  of  the 
hypoglossus.  The  fibers  of  the  nerve  sj^ring  from  the 
numerous  large  multipolar  ganglion  cells.  The  cells  are 
surrounded  by  a  delicate  network  of  coarse  and  fine 
mednllated  nerve-fibers.  Some  of  these  fibers  belong  to 
central  pathways,  others  effect  a  close  connection  between 
the  two  nuclei,  thereby  facilitating  the  consentaneous 
action  of  the  two  halves  of  the  tongue,  and  subserve  the 
transmission  of  reflexes.  The  nuclei  of  the  facial,  oculo- 
motor, etc..  are  in  every  respect  similar  in  structure. 
Thus,  the  peripheral  motor  neuron  begins  in  these  two 
regions,  while  its  cells  are  surrounded  by  the  terminal 
fibrils  of  the  central  neuron;  the  latter  can  not  be  seen 
with  this  stain. 


Tab,  2  4. 


Fig.l. 


Eig,2, 


Ltth.  Anst.  F.  Reichhold.  ifiinrhen . 


Tab.:^:,. 


Mg.l. 


Fig.  3. 


Fiff.3. 


J. I  III.  Afi.sl  h.  RpichhoUl ,  MiiiicJien. 


PLATE  25. 

Fig.  1. — Transverse  Section  through  the  White  Substance 
of  the  Spinal  Cord  (Lateral  Column)  (carmin).  The  white 
substance  is  composed  of  closely  packed  medullated  nerve- 
fibers  of  varying  caliber,  embedded  in  the  neurogliar  or 
sustentacular  substance.  As  most  of  the  nerve-fibers  have 
a  longitudinal  course,  they  appear  in  this  preparation  in 
transverse  section  ("sun  pictures").  The  axis-cylinder 
is  seen  in  the  center  of  each  fiber. 

Fig.  2. — Section  through  a  Spinal  Ganglion  (carmin  stain). 
The  strongly  pigmented  cells  of  the  ganglia,  like  the 
Gasserian  ganglion,  for  instance,  are  surrounded  by  the 
centripetal  and  centrifugal  nerve-fibers  (the  centrifugal 
fibers  correspond  to  the  posterior  roots).  One  fiber  enters 
and  leaves  each  cell  (T-shaped  division).  These  cells  rep- 
resent the  origin  of  the  peripheral  sensory  neuron. 

Fig.  3. — Cross-section  of  a  Peripheral  Nerve  (nigrosin 
stain).  Each  nerve  is  made  up  of  several  bundles.  The 
entire  nerve  is  surrounded  by  an  envelope  of  connective  tis- 
sue, the  epineurium.  The  bundles  are  lodged  in  the  vari- 
ous compartments  of  the  perineurium,  and  the  individual 
nerve  bundles  are  again  subdivided  by  the  endoneurium, 
so  that  each  compartment  of  the  endoneurium  contains 
a  medullated  nerve-fiber  surrounded  by  the  sheath  of 
Schwann  in  a  fibrillary  sheath.  The  perineurium  contains 
the  blood- vessels  and  lymphatics.  Note  the  variable  thick- 
ness of  the  fibers. 


PLATE  26. 

Figs.  1  and  2.  — Diagrammatic  Representation  of  the  Posi- 
tion of  the  Cervical  and  Lumbar  Enlargements.  Between  the 
anterior  longitudinal  sulcus  (S.  a)  and  the  anterior  roots 
{r.  a)  is  the  anterior  column,  which  is  subdivided  into  the 
anterior  (uncrossed)  pyramidal  tract  (Pya)  and  the  ante- 
rior ground  bundle  (/.  a). 

Between  the  anterior  roots  and  the  posterior  roots  (r.  p) 
is  the  lateral  column,  which  is  subdivided  into  Gowers' 
tract  ((r),  the  direct  cerebellar  tract  (Cb),  the  crossed 
lateral  pyramidal  tract  (Pyl),  the  lateral  ground  bundle 
(fal),  and  the  lateral  boundary  zone  (/). 

The  posterior  columns  are  divided  into  the  column  of 
Goll  (G)  and  the  column  of  Burdach  (B).  The  lateral 
posterior  portion  of  Burdach' s  column  corresponds  to  the 
entrance  of  the  posterior  roots  (posterior  (rp)  and  anterior 
(ra)  root  zones).  The  extremities  of  the  posterior  horns 
are  capped  by  the  zones  of  Lissauer  (Z);  v,  central  field  of 
the  posterior  columns.  The  gray  matter  is  divided  into 
anterior  (C.  a)  and  posterior  horns  (C.  p).  Between  them, 
near  the  median  line,  are  the  columns  of  Clarke  (CI).  In 
front  of  the  central  canal  (c.  c)  is  the  anterior  white  (c.  a), 
and  behind  it  the  posterior  gray,  commissure.  The  cells 
in  the  anterior  horn  are  arranged  in  a  mesial  and  a  lateral 
group,  each  of  which  is  again  subdivided  into  an  anterior 
and  a  posterior  segment. 

The  posterior  horn  is  bounded  at  its  base  by  the  sub- 
stantia gelatinosa  (S.  g).  This  is  continuous  with  the 
zona  spongiosa,  which  joins  the  above-mentioned  zone  of 
Lissauer. 

Fig.  3. — The  Central  Canal  and  Adjoining  Structures 
under  a  higher  power.  The  canal  is  lineci  with  cylindric 
epithelium.  We  see  the  medullated  fibers  of  the  anterior 
commissure  (Ca),  which  are  distributed  partly  to  the  an- 
terior column  (fa)  and  partly  to  the  anterior  horn,  and 
the  more  delicate  fibers  of  the  posterior  commissure  (Cp), 
which  radiate  into  the  posterior  horn  and  into  the  posterior 
column.  Sa,  anterior  sulcus  with  the  blood-vessels;  Sp, 
dorsal  septum. 


III. 

TOPOGRAPHIC   ANATOMY 

OF    THK 

NERVOUS  SYSTEM. 

(Plates  27-53.) 


PLATES   54-57,    DIAGRAMMATIC   REPRESENTA 
TION    OF  THE  COURSE  OF  THE  FIBERS. 

(Part  III.  of  Text.) 


Tab.  2. 


PLATE  27. 
Distribution  of  the  Cranial  and  Spinal  Nerves. 

We  determine  the  level  of  the  brain  and  cord  from  which 
the  individual  nerve-roots  arise.  A  detailed  description  of 
the  segments  of  the  brain-stem  and  spinal  cord  is  found  in 
the  text.  (Fig.  13.)  For  the  cutaneous  areas  see  Figure 
21  a  and  b.  A  knowledge  of  the  relation  of  the  individual 
segments  of  the  spinal  cord  to  the  vertebral  column 
(spinous  process)  and  of  the  points  of  exit  of  the  spinal 
nerves  is  of  the  highest  importance.  The  nerves  of  the 
lumbar  region  emerge  some  distance  below  the  segment 
from  which  they  arise.  This  arrangement  and  the  forma- 
tion of  the  plexuses  is  readily  seen  in  this  plate. 

The  segments  are  marked  with  red  numbers,  the  motor 
nerves  are  blue,  the  sensory  brown,  after  their  exit  from 
the  plexus;  the  explanatory  text  is  also  printed  in  the  cor- 
responding colors.  The  ultimate  distribution  of  the  cuta- 
neous sensory  nerves  will  be  best  understood  by  a  study 
of  figures  18,  19,  and  20  in  the  text. 

The  most  important  motor  nerves  are  numbered,  and  in 
the  adjoining  table  the  muscles  innervated  by  the  various 
nerves  and  the  more  important  facts  in  regard  to  their 
function  are  given,  except  in  those  cases  where  the  name 
of  the  muscle  itself  is  sufficiently  expressive. 


{{a)  Internal  eye  muscles  (the  ciliar)*  ganglion   interposed):  Ciliary  m.   for 
accommodation;  sphincter  pupillae  for  contraction  of  pupil. 
(6)  External  eye  muscles  (levator  palp,  super.;  rectus  super.,  intern.,  infer.; 
obliquus  inferior):  rotation  of  eyeball  upward,  inward,  and  downward. 

2.  Superior  oblique  of  the  eye:  rotation  downward  and  outward. 

3.  Muscles  of  mastication  (nia>;seter,  temporal,  pterygoids,  mylohyoid,  digastric 
(ant.  belly),  tensor  tympani,  tensor  et  levator  veli  palati):  lacrimal  secretion  (?). 

4.  External  rectus  of  the  eye:  rotation  outward. 

5.  Facial  muscles  of  expression  (occipitofrontalis,  orbicularis  oculi,  orbicularis  oris, 
zygomatic,  mental,  platysraa,  auriculares,  stapedius,  digastric  (post,  belly),  etc.): 
salivary  secretion,  lacrimal  secretion  (?),  muscles  of  palate  (?). 

6.  Muscles  of  deglutition  (constrictors,  cricothyroid):  gast  ric  secretion  ;  cardiac  and 
respiratory  movements. 

7.  Muscles  of  the  tongue  (sternohyoid,  thyroidei). 

8.  Muscles  of  the  larynx:  phonation.  Muscles  of  the  palate,  pharynx,  esophagus 
(vagus):  act  of  deglutition.  Sternocleidomastoid:  lateral  rotation  and  inclina- 
tion of  the  head.     Trapezii  (in  part):  elevation  of  the  shoulders. 

9.  Posterior  straight  and  oblique  muscles  of  the  head  and  nape  of  the  neck:  eleva- 
tion and  rotation  of  the  head. 

10.  Deep  posterior  and  anterior  muscles  of  the  back  (trapezii,  in  part):  movements 
of  the  head  and  neck, 

11.  Scaleni :  elevation  of  the  ribs ;  respiration.     Longus  colli. 

12.  Diaphragm  :  respiration. 

13.  Deep  muscles  of  the  neck. 

14.  Pectoralis  major:  adduction  and  forward  movement  of  the  arm.  Pectoralis 
minor;  subclavius. 

15.  Levator  scapulae,  rhomboidei  (nerv.  dorsalis  scapulae) :  draw  the  scapulae  inward 
and  upward.  Serratus  anticus  major  (long  thoracic  nerve) :  tixes  the  scapula  and 
rotates  the  arm  and  scapula  (upward  and  outward)  beyond  the  horizontal. 

16.  Supraspinatus:  elevates  the  arm  and  rotates  it  outward.  Infraspinatus,  teres 
minor:  rotate  the  arm  outward. 

17.  Subscapularis,  teres  major:  rotate  the  arm  inward.  Latissimus  dorsi :  adducts 
the  arm  and  draws  it  backward. 

18.  Deltoid  :  elevates  the  arm  to  the  horizontal. 

19.  Biceps,  flexor,  and  supinator  of  the  forearm;  brachialis  anticus,  flexor  of  the 
forearm ;  coracobrachial  is. 

20.  Flexor  digitorum  communis  (radial  portion):  flexes  the  distal  phalanges. 
Flexor  longus  pollicis  (distal  phalanx)  ;  flexor  carpi  radialis  ;  pronator  teres  and 
quadratus;  palmaris  longus;  the  thenar  muscles:  oppose  the  thumb,  flex  the 
proximal,  and  extend  the  distal  plialanx.  Lumbricales  (1,  2,  rarely  3) :  flex  the 
proximal,  and  at  the  same  time  extend  the  distal  phalanges. 

21.  Triceps:  extensor  of  the  forearm.  Brachioradialis,  erroneously  termed  supina- 
tor longus :  flexor  and  pronator  of  the  forearm.  Extensor  digitorum  communis : 
extends  the  proximal  phalanges.  Extensor  pollicis ;  abductor  pollicis ;  supinator 
brevis;  extensor  carpi  radialis  and  ulnaris. 

22.  Flexor  digitorum  profundus  (ulnar  portion),  see  20.  Flexor  carpi  ulnaris; 
hypothenar  muscles;  interossei :  flex  the  proximal  phalanges.  Lumbricales  i3 
and  4),  see  20.     Adductor  pollicis. 

23.  Deep  muscles  of  the  back. 

24.  Intercostal  muscles. 

25.  Deep  muscles  of  the  back  :  extensors  of  the  trunk. 

26.  Itjtercostal  muscles. 

27.  Muscles  of  the  back. 

28.  Intercostal  muscles;  abdominal  muscles  (rectus,  external  oblique):  abdominal 
pressure. 

29.  Dorsolumbar  muscles. 

30.  Transversalis  and  internal  oblique:  abdominal  pressure. 

31.  Cremaster,  transversalis,  oblique. 

32.  Obturator  externus  ;  adductores  femoris  ;  gracilis  :  adductor. 

33.  Psoas  (lumbar  plexus)  ;  iliacus  internus:  elevate  the  thigh  and  flex  the  trunk. 
Quadriceps  :  extensor  of  the  leg.     Sartorius. 

34.  Gluteus  raedius  and  minimus:  abductors  of  the  thigh.  Tensor  fasciae  latae; 
pyriformis  ;  obturator  internus  :  external  rotators. 

35.  Gluteus  maximus:  extensor  of  the  thigh. 

36.  Gemelli;  biceps;  semitendinosus;  semimembranosus:  flexors  of  the  leg.  Quad- 
ratis  femoris  :  external  rotator. 

37.  Tibialis  anticus:  elevates  the  inner  border  of  the  foot.  Peronei :  elevate  the 
outer  border  of  the  foot.     Extensor  digitorum  communis. 

38.  Gastrocnemius;  soleus:  plantar  flexion  of  the  foot.  Flexor  digitorum ;  tibialis 
posticus. 

^Q    I  Small  muscles  of  the  foot  (fle.\or  brevis,  interossei,  etc.). 

41.  Levator  ani,  sphincter  an i  internus,  sphincter  vesicae. 

42.  Sphincter  ani,  perineal  muscles,  bulbocavernosus,  etc. 

43.  Sphincter  ani  externus. 


Serial  Sections  through  the  Central  Organ. 

Plates  28  to  50  contain  frontal  sections,  Plates  33  to  36 
sagittal  and  horizontal  sections,  first  through  the   entire 

hemisphere,  then 
through  the  brain-stem, 
the  medulla,  and  the 
spinal  cord.  The  sec- 
tions are  either  drawn 
or  photographed  from 
actual  preparations 
stained  with  medullary 
sheath  stain,  and  are 
not  in  any  sense  schem- 
atic. The  order  of  suc- 
cession of  the  frontal 
sections  is  shown  in  the 
accompanying  diagram 
of  the  brain-stem,  which 
is  represented  as  though 
flattened  out.  The  or- 
iginally white  medul- 
lary substance  is,  of 
course,  stained  black  in 
all  the  sections.  Unless 
it  is  mentioned  other- 
wise, the  sections  are 
to  be  considered  life- 
size. 

The  student  should 
carefully  reconstruct  the 
entire  series  by  compar- 
ing each  section  with  the 
sections  immediately 
preceding  and  following 
it,  and  noting  the  posi- 
tion on  the  accompany- 
ing diagram. 

[Note.— For  the  cere- 
bral sections  the  brain  of 
a   sixteen-year-old   boy 
was  used.     In  an  adult  brain  the  white  matter  is  more 
massive  and  more  completely  differentiated.] 


41,2 


PLATE  28. 

Fig.  1. — Frontal  Section  through  the  Genu  of  the  Corpus 
Callosum  and  Anterior  Segment  of  the  Frontal  Lobe.  The 
section  includes  the  frontal  lobe  and  its  three  convolutions: 
superior,  middle,  and  inferior  (jr.  -s-,  fr.  ?n,  fr.  i).  The  tip 
of  the  anterior  horn  (v.  a. )  is  seen  in  the  white  substance. 
The  radiation  of  the  corpus  callosum  (Rcc)  connects  all  the 
parts  of  the  frontal  lobe  with  the  corresponding  })arts  of 
the  opposite  side.  Laterally  from  the  anterior  cornu  of 
the  lateral  ventricle  (v. a)  is  the  beginning  of  the  corona 
radiata;  p.Cr,  its  base.  Centrum  semiovale  (C.  Vieuss); 
eg,  cingulum  (association  bundles);  ft,  tangential  fibers; 
St.  s,  central  gray  matter  of  the  ventricle.  On  the  orbital 
surface  the  olfactory  bulb  is  seen  in  transverse  section  (/). 

Fig.  2. — Frontal  Section  through  the  Head  of  the  Caudate 
Nucleus.  Behind  the  genu  of  the  corpus  callosum  is  the 
beginning  of  the  septum  lucidum  (s.  j?);  v,  fifth  ventricle. 
The  cut  head  of  the  caudate  nucleus  is  seen  projecting  into 
the  anterior  horn  (v.  a).  To  the  outer  side  the  most  an- 
terior bundles  of  the  anterior  limb  of  the  inner  capsule 
(c.  i.  a)  are  closely  applied  to  the  lateral  side  of  the  caudate 
nucleus,  in  the  substance  of  which  they  disappear.  Note 
the  more  delicate  structure  of  the  medullary  layer  (cen- 
trum semiovale  Vieussenii)  with  the  interlacing  bundles  of 
fibers:  (1)  The  radiation  of  the  cor|)us  callosum;  (2)  the 
corona  radiata;  (3)  association  bundles:  Fasciculus  occipi- 
tofrontalis  (of);  cingulum  (eg);  fasciculus  arcuatus  (fa); 
fasciculus  uncinatus  (fu). 

ce,  External  capsule;  cl,  claustrum;  ft,  tangential  fibers; 
pesfr.  i.,  base  of  the  third  frontal  convolution;  sL,  nerves 
of  Lancisi;  st.  a.,  central  gray  matter. 


Tab.  28. 


(0%.% 


frontali 
'superior 


Fiy.^. 


Basis 


7hh.2S. 


Full 


FifiJi 


PLATE  29. 

Fig.  1. — Frontal  Section  through  the  Middle  of  the  Septum 
Lucidum.  The  tip  of  the  temporal  lobe  is  also  included 
in  the  section.  In  the  white  matter  the  section  passes 
through  the  corpus  striatum,  more  particularly  the  pu- 
tamen  (Put.)  or  outer  segment  of  the  lenticular  nucleus; 
the  anterior  limb  of  the  capsule  (c.  /.  a)  breaks  through 
the  corpus  striatum  and  thus  divides  it  into  the  caudate 
nucleus  or  mesial  portion,  and  the  lenticular  nucleus  or 
lateral  portion.  To  the  outer  side  of  the  putamen  is  the 
external  capsule  (c.  e);  and  outside  of  the  latter,  the  claus- 
trum  (cl). 

Fig.  2. — Section  through  the  Anterior  Commissure.  The 
descending  crura  of  the  fornix  (/)  make  their  appearance. 
We  also  see  the  inner  segments  (gl.  p,  globus  pallidus)  of 
the  lenticular  nucleus.  At  the  base  of  the  brain  the  sec- 
tion has  passed  through  the  optic  chiasm,  to  the  lateral 
side  of  which  the  olfactory  tubercle  (t.  o)  is  visible.  The 
most  anterior  convolution  of  the  insula  (Ins)  appears  at 
the  bottom  of  the  fissure  of  Sylvius,  laterally  from  the 
claustrum.  In  the  anterior  portion  of  the  temporal  lobe 
we  see  the  beginning  of  the  nucleus  amygdalae  (iV.  am), 
which  is  seen  better  in  the  following  section;  the  cortical 
convolutions  have  been  cut  away.  The  anterior  commis- 
sure (c.  ant)  resembles  the  corpus  callosum  in  that  it  con- 
nects the  temporal  and  occipital  convolutions  on  the  basal 
surface.  Between  the  crura  of  the  fornix  is  seen  the  be- 
ginning of  the  third  ventricle  (v.  III). 

Abbreviations.  — ce,  Capsula  externa,  cia,  capsula  interna 
anterior  ;  eg,  cingulum  ;  cl,  claustrum  ;  fa,  fasciculus 
arcuatus ;  fu,  fasc.  uncinatus  ;  imf  infundibulum  ;  of. 
fasc,  occipitofrontal  is  ;  p  Cr,  foot  of  corona  radiata;  r, 
rostrum  ;  Rcc,  radiation  of  corp.  callos. ;  Sbst.  i,  substan- 
tia innominata  ;  s  L,  strise  Lancisi ;  s  p,  septum  pelluci- 
dum ;  stc,  stria  cornea ;  sts,  substant.  subependymica ; 
Subst.  p.  ant,  Substantia  perforata  anterior ;  tc,  tuber 
cinereum  ;  to,  tuber  olfact. ;  v,  ventriculus  sept,  pelluc. 
(fifth  ventricle);  va,  anterior  horn;  z  B,  Broca's  convo- 
lution ;  /,  tractus  olfactorius. 


Tah.  29. 


\ 


Tab.  :^9. 


Fiq.^ 


T<th.  :iO- 


Tab.  80. 


\c.vJ\   (  ^^-    ^ 

radiala\    Z~st. 


g.cp.  C4!nlr  sfinioiiaU. 


Tw^^y 


/nucL   )) 


Fig.  I. 


PLATE  30. 

Fig.  1. — Frontal  Section  behind  the  Anterior  Commissure.  The  de- 
scending crura  of  the  fornix  (fd)  sweep  backward  to  the  corpus  albi- 
cans at  the  base  of  the  brain.  The  body  of  the  fornix  is  hidden 
underneath  the  corpus  callosum.  (8ee  Fig.  2.)  The  anterior  {na) 
and  lateral  (»7)  nuclei  of  the  optic  thalamus  come  into  view,  and 
between  the  optic  thalami  the  third  ventricle  {v  III )  now  begins  to 
widen  out. 

The  globus  pallidus  {gl.  pall)  subdivides  into  several  segments,  and 
with  its  basal  fibers  (ansa  lentiformis)  surrounds  the  inner  capsule. 
The  optic  tracts  (tr.  II)  x)aas  backward  from  the  chiasm  to  the  lateral 
geniculate  body. 

As  the  anterior  commissure  {c.  a. )  also  arches  backward  at  this 
level,  it  is  seen  in  oblique  section. 

Fig.  2. — Section  through  the  Knee  of  the  Inner  Capsule.  Beneath  the 
most  posterior  portion  of  the  upper  frontal  convolutions  are  the 
central  convolutions,  and  at  the  bottom  of  the  fissure  of  Sylvius  {f.  S) 
the  convolutions  of  the  insula  {ins).  In  the  temporal  lobe  (three 
convolutions)  the  nucleus  amygdalae  (iV.  a)  has  come  into  view,  and 
to  its  mesial  side  tlie  cornu  ammonis  (c.  Am),  which  represents  the 
inner  bulging  of  the  Hippocampal  convolution.  The  caudate  nucleus 
(n.  c.)  is  separated  from  the  optic  thalamus  by  the  stria  cornea.  The 
fibers  of  the  ansa  lentiformis  {ansa  It),  which  are  derived  from  the 
globus  pallidus  {gJ.  pall),  pass  around  and  through  {x)  the  lowest  bun- 
dles of  the  knee  of  the  inner  capsule;  a  part  of  these  fibers  are  collected 
into  a  bundle  in  the  subthalamic  region  and  pass  to  the  lower  field  of 
the  tegmentum  (h^^). 

The  optic  thalamus  (7'^)  is  joined  by  the  inferior  peduncle  of  the 
thalamus  {ped.  inf.  th,  see  Fig.  1),  derived  from  the  temporal  lobe,  and 
situated  underneath  the  ansa  lentiformis,  with  which  it  combines  to 
form  the  ansa  peduncularis.  The  optic  thalamus  has  greatly  increased 
in  size,  and  w  ith  its  upper  portion  {tuhei'culum  ant.  na. )  reaches  to  the 
fornix. 

It  is  divided  into  three  nuclei:  the  anterior  {na),  lateral  {nl),  and 
mesial  (nw).  To  its  outer  side  lies  the  lamina  medullaris  externa 
{Im),  and  between  this  and  the  inner  capsule  the  zona  radicularis  {zr). 

Ahhreviations.  —  c.  Tailpiece  of  caud.  nucl. ;  e  M,  commissura  Mey- 
nert;  fd,  descending  fornix;  fli,  descending  long,  bundle;  Ima,  lamin. 
medullar,  externa  of  lentic.  nucleus;  Imi,  lam.  medull.  interna;  o,  optic 
radiation ;  Sc,  substantia  grisea  centralis  (central  gray  matter) ;  str.  z, 
stratum  zonale  thalami;  t,  tapetum;  r1,  lateral  ventricle;  n,  descending 
horn;  v  III,  third  ventricle.     For  other  abbreviations  see  Plate  29,  8. 


PLATE  31. 

Fig.  1. — Section  through  the  Middle  of  the  Third  Ventricle.  We  see  the 
three  nuclei  of  the  optic  thalamus  ( Thai,  o)  shown  on  Plate  30.  From 
the  upper  (w.  a)  the  bundle  of  Vicq  d'Azyr  {v.  A)  passes  downward  to 
the  corpus  albicans  [cp.  m).  Underneath  the  optic  thalamus  the  sub- 
thalamic region  comes  more  plainly  into  view;  the  latter  consists  of  the 
ansa  lentiformis  {al)  and  the  tegmental  portion  from  the  ventral  part 
of  the  optic  thalamus.  It  is  divided  into  an  upper  {fh^)  and  a  lower 
ifh^^)  tegmental  field,  having  between  them  the  zona  incerta  {zi)  or 
continuation  of  the  zona  radicularis  thalami  {zr),  and  containing  be- 
sides the  body  of  Luy  (subthalamic  body)  (cl).  The  internal  capsule 
(in  the  region  of  the  niost  anterior  segment  of  the  posterior  limb)  {c.i.p) 
becomes  gradually  reinforced  by  constant  additions  from  the  central 
convolutions  (motor  central  neurons);  the  mesial  portion  is  beginning 
to  appear  at  the  base  of  the  hemisphere  at  the  crusta  or  pes  (P).  The 
lenticular  nucleus  has  diminished  in  size.  The  descending  horn  {v.  i) 
in  the  temporal  lobe,  on  the  other  hand,  has  increased.  The  optic 
tract  {tr.  o)  is  seen  underneath  the  crusta,  which  now  projects  freely. 
The  fornix  (/)  terminates  laterally  in  the  corpus  albicans  {cp.  m.). 

Fig.  2. — Section  through  the  Central  Convolutions.  The  subdivision 
of  the  optic  thalamus  into  its  upper  or  anterior  (na),  lateral  {nl),  and 
mesial  {nm)  nuclei  is  plainly'  seen.  Between  the  two  latter  nuclei 
are  the  fibers  of  the  lamina  mexluUaris  interna  (mi].  On  the  other 
side  the  capsule  is  bounded  by  the  zona  radicularis,  which  is  formed  by 
fibers  entering  from  the  internal  capsule.  The  subthalamic  region  be- 
tween the  crusta  and  the  optic  thalamus  has  widened  out.  It  contains 
the  corpus  subthalamicum  or  body  of  Luy  (c.  L),  the  red  nucleus  {n,.  r) 
and  its  lateral  w^hite  matter  (H,  and  the  zona  incerta  {z.  i).  Imme- 
diately beneath  is  the  beginning  of  the  substantia  nigra  (Sn).  In  the 
median  line  the  first  fibers  of  the  oculomotor  (III)  begin  to  emerge. 

In  the  descending  horn  {v.  i)  the  tailpiece  of  the  caudate  nucleus  (c), 
which  is  reflected  toward  the  base  of  the  brain,  is  also  included  in  the 
section.  The  mesial  wall  of  the  lateral  ventricle  is  formed  by  the  cornu 
ammonis,  gyrus  dentatus  (gd),  fimbria  (/),  and  inferior  choroidal 
plexus  ipl);  the  lateral  wall  is  formed  by  the  tapetum  (tp). 

Abbreviations. — ce,  Capsula  externa;  eg,  genu  capsulae  int.;  cp, 
capsul.  int.  (posterior  limb);  cl,  claustrum;  fa,  fascicul.  arcuatus;  fu, 
fasc.  uncinatus;  ^^/,  inferior  long,  bundle;  gl.  p.,  globus  pallidus;  m\ 
caudate  nucleus;  ?if,  cup-shaped  nucleus  of  Flechsig;  of,  fasc.  fronto- 
occipital. ;  o,  optic  radiation;  2)  Cr,  foot  of  corona  radiata;  Put,  puta- 
men;  Rcc,  radiation  of  corp,  callos. ;  s,  subst.  subependymica;  sc, 
stria  cornea;  sp,  septum  pellucidum;  tt,  taenia  thalami;  v.  lat.,  lat- 
eral ventricle;  vi,  descending  horn;  v.  Ill,  third  ventricle;  x,  point 
where  the  ansa  lentiformis  traverses  the  inner  capsule. 


'^Centr  semiot'ale 


Tab.  31. 


%r    - 

^   Uncus  (Uncus'- — ^ 

n.oJiujyd^      \q  ^^^    c.Amonis 

^  fcMtonisj'XlU  '    ^         S:^t_-^«^ 

\g.HipPocampt 
Fig.  1. 


'lah.M. 


Fig.  2, 


Tabr. 


Fifj.l. 


Fiq.^. 


Tab.  32. 


Pi^.  1. 


Fig.£. 


PLATE  32. 

Fig.  1. — Section  through  the  Pulvinar  Thalami.  The  brain-stem 
emerges  more  and  more  from  the  hemisphere.  The  cerebral  peduncle 
{Ped)  is  entirely  free,  while  the  pulvinar  is  still  attached  by  its  upper 
and  posterior  peduncles.  Wedged  in  between  the  cerebral  peduncle 
and  the  internal  capsule  ( posterior  segment,  cirl)  we  find  the  lateral 
geniculate  body  {v.  g.  /),  in  which  the  optic  tract  [tr.  o)  terminates,  and 
the  mesial  geniculate  body  (c.  g.  m). 

The  descending  horn  (r.  /)  is  apparently  opened  up  so  that  its  for- 
mation by  the  invagination  of  the  cortex  of  the  hippocampal  convolu- 
tion is  readily  seen.  From  the  free  border  of  the  latter  the  fimbria 
(/)  begins  its  course  upward.  To  the  outer  side  of  the  lateral  genicu- 
late body  the  optic  radiation  (o)  begins  in  the  triangular  field  of  Wer- 
nicke («')  and  passes  to  the  cortex  of  the  occipital  lobe.  The  subthal- 
amic region  ha»s  been  replaced  by  the  important  tegmental  region;  the 
subthalamic  body  has  disappeared,  the  fillet  (upper,  Is,  and  lower,  li) 
has  increased  in  width,  and  the  red  nucleus  {n.  r)  has  become  larger. 
The  third  ventricle  is  about  to  become  the  aqueduct  of  Sylvius.  The 
peduncular  fibers  nearest  the  median  line  are  surrounded  by  the  first 
transverse  fibers  of  the  pons;  the  lenticular  nucleus  has  disappeared. 

Fig.  2. — Section  through  the  Parietal  Lobe.  The  brain-stem  together 
with  the  pulvinar  is  completely  separated  from  the  hemisphere.  The 
picture  resembles  the  first  section  through  the  frontal  lobe. 

The  section  includes  the  splenium  of  the  corpus  callosum;  the 
tapetum  (//>),  to  the  lateral  side  of  the  posterior  horn  of  the  lateral  ven- 
tricle {v.  p);  the  optic  radiation  (o),  which  passes  from  the  primary 
optic  centers  (lateral  geniculate  body,  inferior  corpora  quadrigemina, 
pulvinar)  to  the  occipital  lobe.  To  its  outer  side  is  the  inferior  longi- 
tudinal bundle  (fli). 

Abbreviations. — c,  Cauda;  c.  ex,  capsula  externa;  eg,  cingulum;  cirl, 
capsula  intern,  retrolenticularis;  cm,  cella  media;  d,  diverticulum  subi- 
culi;/c,  fasciola  cinerea;/m, foramen  caecum  anterius ;./?/,  inferior  long, 
bundle;  fnia,  forceps  major;  fmi,  forceps  minor;  fp,  posterior  long, 
bundle;  gd,  gyrus dentatus;  me,  lamina medullaris  externa;  nc,  caudate 
nucleus;  w/,  nucleus  lateralis;  of,  fasc.  fronto-occipital. ;  pi,  plexus 
choroideus  inferior;  Py,  fibers  of  •pyramids;  Ecc,  radiation  of  corp. 
callos. ;  s,  accessory  fillet;  Sn,  substantia  nigra;  t,  taenia  tecta;  fp, 
tapetum;  tt,  taenia  thalami;  vl,  lateral  ventricle;  v  III,  third  ventricle; 
zr,  zona  radicularis. 


PLATE  33. 

Fig.  1.  — Section  through  the  Occipital  Lobe.  The  cortical  visual 
ceuter  lies  chiefly  in  the  neighborhood  of  the  c^lcarine  fissure  in  the 
cuneus  and  lingula.  Here  the  fibers  of  Gratiolet's  optic  radiation  (o) 
gradually  make  their  entrance.  The  association  fibers  are  represented 
by  the  inferior  longitudinal  bundle  {Is),  the  fasciculus  transversus 
cunei  {t),  and  the  stratum  calcarinum  (str). 

Ahhreviations. — c,  Remains  of  the  forceps  of  the  corpus  callosum;vp, 
remains  of  the  posterior  horn  of  the  ventricle. 

Fig.  2, — Sagittal  Section  through  the  Brain-stem  (two  millimeters  to 
one  side  of  the  median  line).  The  section  shows:  The  optic  thalamus 
(inner  wall  of  the  third  ventricle,  v.  Ill),  the  posterior  commissure  (cp), 
the  anterior  and  posterior  corpora  quadrigemina  {cqa  and  cgp)  with  the 
central  gray  matter  of  the  aqueduct  (c),  from  which  the  oculomotor 
(///)  arises.  Underneath  is  the  tegmental  region  containing  the 
red  nucleus  (Mr),  the  decu.ssation  of  the  brachia  (dbr),  and  the  ante- 
rior brachium  which  passes  from  that  point  to  the  cerebellum ;  I.  m, 
fillet.  In  the  pons  is  the  pyramidal  tract  {Fyr)  which  emerges  as  the 
pyramids  {Py).  Above  the  pyramidal  tract  the  trapezoid  body  {ctz) 
in  transverse  section,  and  above  the  pyramid  the  olive  (o/.  inf).  Be- 
neath the  floor  of  the  fourth  ventricle  {ventr.  IV)  are  the  following 
structures:  The  locus  coeruleus  (?c),  the  knee  of  the  facial  nerve 
{g.  VII )  with  the  nucleus  of  the  abducens  immediately  beneath  it, 
the  fibers  of  this  nerve  (  VI )  passing  down  to  the  base  of  the  brain, 
the  dorsal  longitudinal  bundle  {fd),  and  the  striae  acusticae  {st.  o). 
In  the  medulla  oblongata  the  nucleus  of  the  hypoglossus  (w,  XII),  the 
funiculus  gracilis  (nucleus  of  Goll,  n.  G),  the  internal  arcuate  fibers 
ifai),  the  posterior  ( fp)  and  anterior  ( fa )  columns  of  the  spinal  cord, 
and  the  decussation  of  the  pyramids  {D.  pyr).  We  see  also  IV, 
trochlear  nerve;  Ch,  chiasm;  cpw,  corpus  albicans;  fr,  fasciculus  retro- 
flexus;  tc,  tuber  cinereum;  tt,  taenia  thalami;  r,  bundle  of  Vicq  d'Azyr. 

Fig.  3. — Sagittal  Section  through  the  Brain-stem  and  Corpus  Callosum 
(six  millimeters  to  one  side  of  the  median  line). 

Ahhreviations. — al,  Ansa  lentiformis;  c.  rfew^ ,  corpus  den tatum ;  c  L, 
corpus  Luys;  e.  rst,  corpus  restiforme;  fs,  fasciola  cinerea;  Jl,  floccu- 
lus; fh^,  Forel's  tegmental  bundle;  /.  sup.  a,  lobus  superior  anterior; 
II,  Im,  laqueus  lateralis  and  laqueus  medialis;  m,  motor  nucleus  of  fifth 
nerve;  «r,  nucleus  ruber;  Py,  pyramidal  tract;  qa,  qp,  anterior  and 
posterior  corp.  quadrigemina;  s,  sensory  nucleus  of  fifth  nerve;  Sn, 
substantia  nigra ;   V,  trigeminus. 


Tab.  38. 


Tah.:i^. 


Fixf.L 


^^^1 


-/■^ 


7ah.:i^. 


jS^^T^'^^] 


ritj.i. 


Fiq.B. 


Fig.S 


Tab.  34. 


^^. 


t /7^c/J  g cenl£ant./l)\(7.centrpist.       \ ppaneUnr 
Fig.  1, 


Vh,. 


Fiy,  3. 


PLATE  34. 

Fig.  1. — Horizontal  Section  Immediately  above  the  Corpus 
Callosum.  The  lateral  ventricle  (ventr.  lat.)  is  laid  open 
from  above;  the  section  passes  through  the  foot  of  the 
corona  radiata. 

Fig.  2. — Horizontal  Section  through  the  Center  of  the  Cor- 
pus Callosum.  The  caudate  nucleus  and  optic  thalamus 
are  cut  near  the  surface.  To  either  side  we  see  the  inner 
capsule  (anterior  limb,  cia),  knee  (g),  posterior  limb  (cip), 
and  the  outer  segment  of  the  lenticular  nucleus  of  which 
the  putamen  is  seen  between  the  fibers  of  the  capsule.  To 
the  outer  side  of  the  latter  is  the  foot  of  the  corona  radi- 
ata (pes  Cor.  rad). 

Fig.  3. — Horizontal  Section  Immediately  below  Figure  2, 
The  putamen  has  increased  in  size;  the  most  posterior 
segment  of  the  inner  capsule,  the  pars  retrolenticularis 
(dH),  has  come  into  view  and  is  joined  by  Gratiolet's  optic 
radiation  {Ro)]  to  the  outer  side  is  the  inferior  longitu- 
dinal bundle  {fll)]  to  the  mesial  side,  the  tapetum  (tap), 
which  forms  the  lateral  wall  of  the  posterior  horn. 

Abbreviations. — c,  Tailpiece  of  the  caudate  nucleus;  c. 
call,  corpus  callosum;  cex,  external  capsule;  cia,  internal 
capsule  (anterior  limb);  cirl,  internal  capsule,  pars  retro- 
lenticularis; cip,  internal  capsule  (posterior  limb);  cl, 
claustrum;  fd,  descending  limb  of  the  fornix;  fli,  inferior 
longitudinal  bundle;  fma,  forceps  major;  g,  knee  of  the 
inner  capsule;  gf,  gyrus  fornicatus;  me,  lamina  medul- 
laris  externa;  mi,  lam.  med.  interna;  na,  nucleus  anterior; 
nl,  nucleus  lateralis;  nm,  nucleus  medialis;  of,  fascicul. 
occipitofrontalis;  p  Gr,  foot  of  corona  radiata;  pi,  plexus 
choroid,  lat.;  pp,  pedunculus  post,  thalami;  Ro,  optic 
radiation;  sg,  substant.  grisea  subependymica;  sc,  stria 
cornea;  si,  striae  Lancisi;  sp,  septum  pellucidum;  sz, 
stratum  zonale;  t,  taenia  tecta;  tap,  tapetum;  v,  fifth 
ventricle;  v.  ant,  anterior  horn;  vl  post,  posterior  horn; 
2/-,  zona  radicularis. 


PLATE  35. 

Fig.  1. — Horizontal  Section  through  the  Middle  of  the  Optic 
Thalamus. 

Figs.  2  and  3. — Sections  through  the  Base  of  the  Optic 
Thalamus.  For  lettering  not  included  in  the  next  para- 
graph see  Plate  34. 

Abbreviations. — /*.  A,  Cornu  animonis;  ca,  anterior  horn; 
cm,  cella  media;  cp,  commissura  posterior;  E,  pineal 
gland;  /,  fornix;  fh',  Forel's  tegmental  bundle;  fmi,  for- 
ceps minor;  g,  central  gray  matter;  gd^  gyrus  dentatus; 
gl.  pall,  globus  pallidus;  gscc,  gyrus  subcallosus;  Ime,  Imi, 
lamina  medullaris  ext.  and  interna  of  lenticular  nucleus; 
nf,  cup-shaped  nucleus  of  Flechsig;  pm,  plexus  choroid, 
med.;  Pidv,  pulvinar  thalami;  r,  fascicul.  retroflexus;  spl 
cCj  splenium;  tt,  taenia  thalami;  v,  bundle  of  Vicq  d'Azyr; 
V  III,  third  ventricle;  w,  Wernicke's  lateral  field  of 
pulvinar. 


Tab.  35. 


Fi(j.  ^. 


Ffff.  S. 


7ah.3o. 


Fig.3. 


LUh.  Anst  F.  Reichhold,  Mimchen. 


PLATE  36. 

Figs.  1  to  3. — Horizontal  Sections  through  the  Subthalamic 
Region  and  Corpora  Qiiadrigemina.  In  these  sections  the 
pes  separates  from  the  hemisphere  as  the  continuation  of 
the  posterior  limb  of  the  capsule;  the  posterior  commis- 
sure makes  its  appearance. 

For  the  lettering  not  included  in  the  following  paragraph 
see  Plates  34  and  35. 

Abbreviations. — ^,  AquseductusSylvii;  al,  ansa  lentifor- 
mis;  6a,  brachiumanticum;  bp,  brachium  posticum;  cant, 
commissura  anterior;  sg,  central  gray  matter;  cing,  cing- 
ulum;  cm,  corpus  mammillare;  fh",  field  h"  of  tegmen- 
tum (ansalenticularis);  fa,  fasciculus  uncinatus;  g,  central 
gray  matter  of  third  ventricle;  gfr.i,  gyrus  frontalis  infe- 
rior; gl,  corpus  geniculatum  lateral;  gl.p,  globus  pallidus; 
gti,  gyrus  temporalis  inferior;  gts,  gyrus  temporalis  supe- 
rior; gm,,  corpus  geniculatum  mediale;  //,  laqueus  lateralis; 
Im,  laqueus  medialis;  It,  lamina  terminalis;  N III,  fibers 
of  oculomotor;  N  IV,  decussation  of  trochlear  nerve;  nr, 
nucleus  ruber;  p,  fascicul.  longitud.  posterior;  rcc,  rostrum 
corpor.  callosi;  s,  accessory  fillet;  Sb.  in,  substantia  in- 
nominata;  Spa,  Spp,  substantia  perforata  anterior  and  pos- 
terior; tc,  tuber  cinereum;  tro,  tractus  opticus;  ex,  point 
where  ansa  lentiformis  traverses  the  knee  of  the  internal 
capsule;  zB,  Broca's  convolution;  zi,  zona  incerta. 


Tab.  86. 


Tab.Mi 


Fig.J. 


7ah.-n 


Fig.l 


LUh.  Artst  E  Reicfihold,  Miinchen. 


PLATE  :37. 

Fig.  1. —  Vertical  Section  throuyh  the  Anterior  Corpora  Quadriyemina 
and  Puhinar.  The  optic  thalami  (pulviuar)  are  widely  separated  by 
the  anterior  quadrigemina.  Above  the  corpora  quadrigeinina  is  the 
pineal  gland  {E),  above  that  the  large  vein  of  Galen  (??)  and  the  tela 
choroidea  (t.  eh),  and  above  this,  finally,  the  splenium  of  the  corpns 
callosum  and  fornix. 

In  the  central  gray  matter  (c)  the  aqueduct  of  Sylvius  {A),  with 
the  nucleus  of  the  oculomotor  (///)  beneath  it  and  the  nasal  root  of 
the  fifth  nerve  {n)  on  its  lateral  side. 

In  the  corpora  quadrigemina  we  distinguish  a  superficial  (s),  a 
middle  (  w) ,  and  a  deep  (/)  layer  of  white  matter.  Under  these  layers 
are  the  tegmentum  and  the  red  nucleus  [n.  r),  which  approach  each 
other  from  either  side  ;  to  their  outer  side  is  the  upper  sensory  fillet 
[I.  w),  which  is  joined  by  the  lower  fillet  {I.  I)  from  the  corpora  quad- 
rigemina and  the  posterior  brachium  {hp).  To  the  lateral  side  of  these 
structures  we  find  the  mesial  (c.  g.  m.)  and  lateral  {c.  g.J)  geniculate 
bodies.  Separated  from  the  tegmentum  by  the  substantia  nigra,  which 
is  recognized  by  its  darkly  pigmented  cells,  is  the  crusta  (pedunculus), 
which  contains  in  its  central  portion  the  motor  pyramidal  tract  {fpy). 
The  optic  tract  {tr.  o)  paSvSes  to  the  lateral  geniculate  body,  the  anterior 
corpus  quadrigeminum,  and  finally  to  the  pulvinar,  where  it  ends.  From 
this  point  the  fibers  of  the  optic  radiation  {Ro)  pass  through  the  lateral 
white  matter  {w)  toward  the  center  and  finally  to  the  occii)ital  lobe. 
For  further  details  see  the  photograph  on  Plate  40,  2. 

Fig.  2. — Section  between  the  Anterior  and  Posterior  Corpora  Quad- 
rigemina. The  tegmental  region  is  completely  separated  from  the 
pulvinar  and  lateral  white  matter.  The  fillet  {Im,  upper,  and  It,  lower 
lateral)  passes  toward  the  base  of  the  brain  beneath  the  red  nuclei  (»r). 
From  the  depths  of  the  white  matter  (i)  the  fountain-like  tegmental 
radiation  (/./)  rises  to  the  median  line,  where  the  fibers  decussate  in 
Meynert's  tegmental  decussation  (xM)  in  the  raphe.  Immediately 
beneath  the  nucleus  of  the  oculomotor  (n.III)  in  the  central  gray 
matter  (c)  is  the  posterior  longitudinal  bundle  (/),  which  can  be 
plainly  recognized  in  this  section.  On  its  outer  side  fibers  from  the 
optic  thalamus  are  seen  passing  to  the  substantia  reticularis  {Srt).  The 
divisions  of  tlie  oculomotor  nucleus  (ventral  and  dorsal  nuclei)  can  be 
seen.  The  posterior  brachium  (6r.  p)  contains  fibers  running  from  the 
posterior  corpus  quadrigeminum  to  the  mesial  geniculate  body.  Fibei>s 
coming  from  the  striate  body  end  in  the  substantia  nigra.  The  fillet 
which  unites  the  corpora  quadrigemina  with  the  optic  thalamus  {It) 
contains  fibers  which  pass  from  the  anterior  nucleus  in  the  corpora 
quadrigemina  to  the  optic  thalamus.  The  crusta  contains  the  following 
structures:  The  lateral  (oval  or  Tiirck's)  bundle  (fl),  the  pyramidal 
tract  (fpy^i  and  the  mesial  pontine  bundle  (fin).  The  latter  is  sur- 
rounded by  the  accessory  tract  of  the  fillet,  Spitzka's  bundle  from  the 
pyramidal  tract,  which  is  regarded  as  the  central  pathway  of  the  motor 
cranial  nerves;  the  central  pathway  of  the  sensory  cranial  nerves  is 
supposed  to  correspond  to  the  scattered  bundle  of  the  fillet  (rf)  which 
descends  from  the  fillet  to  the  highest  segment  of  the  pes. 

Abbreviations. — c.  call,  Corpus  ciiUosum;  cirl,  capsule  int.  retro- 
lenticularis;  eg,  cingulum;  E,  pineal  gland;  fc,  Forel's  tegmental 
decussation;^?',  fascicul.  longitud.  inf.;  fore,  ma,  forceps  major;  Ir, 
lateral  white  matter  of  red  nucleus;  «,  nasal  or  upper  root  of  fifth  nerve; 
nc,  nucl.  caudatus;  nv,  nucleus  ventralis  thalami;  N.  Ill,  oculomotor; 
of,  fascicul.  occipitofrontalis;  pi  I,  pl.  i,  plexus  choroideus  lateralis, 
inferior;  tp,  tapetum;  f,  taenia  tecta;  so,  stria  cornea;  si,  striae  Lancisi; 
sz,  stratuni  zonale;  r,  vena  magna;  /•.  i)if,  descending  horn;  zr,  zona 
radical  is. 


PLATE  38. 

Fig.  1. — Section  through  the  Posterior  Corpora  Quadrigemina.  On 
the  basal  aspect  the  section  includes  the  anterior  portions  of  the  x)ons 
which  surround  the  crusta.  The  posterior  corpora  quadrigemina  (q.  p) 
are  joined  by  a  part  of  the  inferior  lateral  fillet  (//).  By  the  side  of 
the  nasal,  descending  root  of  the  trigeminus  (w)  we  see  the  trunk  of 
the  trochlear  nerve  {IV),  which  begins  at  this  point.  The  tegmentum 
contains  the  decuasation  {dbr)  of  those  fibers  of  the  brachia  (6r)  which 
arise  in  the  red  nuclei  and  enter  the  cerebellum  (processus  cerebelli  ad 
corpora  quadrigemina) . 

The  posterior  longitudinal  bundle  ( / )  comes  in  relation  on  its  outer 
side  with  the  substantia  reticularis  tegmenti  {Srt).  Underneath  the 
decussation  of  the  brachia  is  the  superior  horizontal  fillet '  Im)  connect- 
ing the  cortex  and  optic  thalami  (central  sensory  pathway),  and  to  the 
outer  side  of  the  latter  the  inferior  fillet  {11}  from  the  corpora  quad- 
rigemina (central  auditory  pathway). 

Most  of  the  peduncular  fibers  end  in  the  pontine  ganglia,  mesial  and 
lateral  pontine  tracts  (  fm,  fl).  The  pyramidal  tract  {f2)y)  only  passes 
through. 

Fig.  2. — Section  through  the  Middle  of  the  Pons.  The  aqueduct  has 
widened  out  and  become  the  fourth  ventricle  (r.  IV).  Its  roof  at  this 
point  is  formed  by  the  anterior  medullary  velum  {v.  m.  a)  and  the 
lingula  (/)  (from  the  vermiform  process  of  the  cerebellum),  and  to 
either  side  by  the  massive  brachia  (6r),  which  have  just  emerged  from 
their  decussation. 

In  the  tegmental  region  we  see  the  posterior  longitudinal  bundle 
(/);the  substantia  reticularis  {Srt),  to  the  lateral  side  of  the  raphe 
(i?),  in  which  numerous  central  pathways  undergo  decussation  ;  the 
central  tegmental  pathway  (cO ;  superior  (mesial)  and  inferior  (lateral) 
fillets  {I.  m  and  /.  I).  Embedded  among  these  fibers  are  numerous 
nuclei  (upper  olive  (o.  s),  nuclei  of  the  substantia  reticularis,  etc.)  ; 
to  the  lateral  side  of  the  tegmentum  the  motor  (m)  and  sensory  (s) 
nuclei  of  the  fifth  nerve  and  its  roots,  which  are  joined  above  by  the 
nasal  (motor?)  root  of  the  fifth  nerve  {n)  (near  the  latter  the  pigmented 
cells  of  the  locus  coeruleus,  li).  It  is  further  reinforced  by  a  bundle  of 
fibers  from  the  neighboring  white  matter  of  the  cerebellum  corre- 
sponding to  the  direct  sensory  cerebellar  tract  (sc),  and  by  a  crossed 
bundle  (e)  from  the  nucleus  of  the  opposite  side.  The  sensory  caudal 
root  of  the  fifth  nerve  (  V.  c)  passes  downward. 

The  pyramids  {Py)  pass  from  the  crusta  through  the  pons  covered 
by  the  superficial  and  deep  pontine  fibers.  The  processus  cerebelli  ad 
pontem  {Prp)  begin  in  the  cerebellar  cortex  {Cb.  cort)  and  terminate  in 
the  pontine  ganglia  of  the  opposite  side  after  decussating  in  the  raphe 
{B).  They  communicate  with  the  mesial  and  lateral  pedunculopontine 
pathway. 

Abbreviations. — A,  aqueduct  of  Sylvius  ;  c,  central  gray  matter  ; 
ctrp,  corpus  trapezoides  ;  <?,  scattered  bundles  of  fillet;  B,  raphe 
(decussation) ;  .s,  jiccessory  fillet. 


Tab.JiS^ 


Tab.  H9. 


PLATE  39. 

Fig.  1. — Section  through  the  Posterior  Extremity  of  the  Pons.  In  the 
tegmentum  the  niiclei  of  the  facial  [n.  VII)  and  abducens  (n.  VI) 
have  made  their  appearance.  The  fibers  of  the  facial  ( VII) ,  after  sur-. 
rounding  the  nucleus  of  the  abducens,  as  shown  on  the  right-hand 
side,  collect  into  a  compact  bundle  at  the  knee  ig)  and  pass  first  hori- 
zontally, and  then  downward  to  emerge  at  the  medulla  ( VII) ;  the 
course  of  the  abducens  is  more  simple.  Its  nucleus  is  connected  with 
the  superior  olive  (o.  s). 

Srt,  substantia  reticularis;  Lm,  superior  fillet;  //,  inferior  fillet, 
etc.,  as  heretofore.  The  caudal  descending  root  of  the  trigeminus 
{V.  c)  joins  with  the  sensory  root  and  passes  downward  by  the  side  of 
the  trunk  of  the  facial  nerve.  To  the  outer  side  the  broad  processus 
cerebelli  ad  pontem  {pr.  p)  appear  with  the  restiform  bodies  (er)  lying 
between  them  and  the  brachia,  as  will  appear  more  plainly  in  the  next 
section. 

Fig.  2. — Section  through  the  Nuclei  of  the  Auditory  Nerve.  In  the 
white  matter  of  the  cerebellum  [Ch)  the  section  has  passed  through  the 
corpus  dentatum  (c.  d),  and  in  the  white  matter  of  the  vermiform 
process  through  the  tegmental  [n.  t)  and  other  nuclei.  The  auditory 
nerve  (  VIII),  makes  its  entrance  to  the  mesial  side  of  the  flocculus 
(Ft).  The  cocidear  branch  {VIII  c)  terminates  in  the  ventricular 
auditory  nucleus  {n.  VIII  c)  to  the  lateral  side  of  the  restiform  body 
(c.  r)  (shown  schematically  on  the  right-hand  side);  the  vestibular 
branch  (n.  VIII  v)  ends  in  the  dorsal  nucleus  of  the  auditory  nerve 
{n.  VIII  d)  and  in  Deitcrs'  nucleus  (n.  D)  or  continuation  of  the  locus 
coeruleus.  From  the  ventral  nucleus  of  the  auditory  nerve  the  trape- 
zoid body  (c.  tr)  passes  transversely  through  the  mesial  (L.  s)  fillet  to 
the  lateral  fillet  (11)  of  the  other  side,  also  to  the  superior  olive  (o.s); 
another  portion  of  the  central  auditory  pathway  reaches  the  same  region 
by  way  of  the  strise  acusticae.  (See  Plate  42. )  The  pyramids  [Py) 
have  emerged  from  the  pons.     Beginning  of  the  inferior  olive  (o.  i. ). 

Abbreviations. — ftr,  Brachium;  erf,  corpus  dentatum  cerebelli;  ct,  cen- 
tral tegmental  tract;  ctr,  corpus  trapezoides;  e,  embolus;  /,  fasciculus 
longitudinalis  posterior;  g,  nucleus  globosus;  n.  D,  nucleus  Deiters  et 
Beciiterew ;  Prp,  processus  cerebelli  ad  pontem ;  E,  raphe ;  s.  C,  direct 
sensory  cerebellar  tract  (Edinger);  sg,  substantia  gelatinosa;  Srt, 
substantia  reticularis  tegmenti ;  vi,  vs,  vermis  inferior  and  superior ; 
!'.  IV,  fourth  ventricle. 


PLATE  40. 

Fig.  1. — Section  through  the  Right  Optic  Thalamus  at  the 
Level  of  the  Middle  Commissure  (behind  the  section  shown 
on  Plate  31,  Fig.  1).  The  three  nuclei  of  the  optic  thala- 
mus are  easily  recognized  (nucl.  anterior,  a;  medial.,  m; 
lateral.,  I).  A  robust  bundle  of  fibers  (y),  known  as  the 
bundle  of  Vicq  d'Azyr,  passes  from  the  anterior  nucleus 
(which  is  shown  in  transverse  section  in  Plates  35  and  36) 
downward  to  end  in  the  corpus  albicans  of  the  same  side 
(its  termination  is  clearly  shown  in  the  unstained  section 
2,  Plate  12).  Underneath  the  optic  thalamus  is  the  sub- 
thalamic region  with  the  ansa  lenticularis — Forel's  field, 
h"  of  the  tegmentum  {An.  I);  subthalamic  body  (c.  L), 
the  fibers  of  which  after  traversing  the  internal  capsule  (ci) 
terminate  in  the  globus  pallidus  (gl.p)  of  the  lenticular 
nucleus;  underneath  is  the  substantia  nigra  (S.  n).  P,  pes. 

The  lateral  zone  of  the  lateral  nucleus  (zona  reticularis) 
is  joined  by  the  corona  radiata  coming  from  the  internal 
capsule  (c.  /).  The  middle  commissure  (c.  m)  contains 
only  a  few  nerve-fibers. 

Fig.  2. — Section  through  the  Anterior  Corpora  Quadrigem- 
ina  on  the  Left  Side  (in  front  of  the  section  shown  on 
Plate  37,  Fig.  1).  The  lateral  geniculate  body  (c.  g.  I) 
and  anterior  corpus  quadrigeminum  (c.  q.  a)  contain 
numerous  terminal  fibrils  from  the  fibers  of  the  optic 
nerve  (tro).  The  pathway  for  the  pupillary  reflex  must 
be  sought  in  this  region,  between  this  point  and  the  oculo- 
motor nucleus  {N  III).  The  emerging  oculomotor  fibers 
{III)  mark  the  beginning  of  the  crusta  or  pes  {Ped).  Its 
mesial  segment  contains  Spitzka's  accessory  bundle  {s), 
which  probably  contains  the  central  pathway  for  the  motor 
cranial  nerves,  and  passes  from  the  pes  upward  to  the  teg- 
mentum to  undergo  decussation  later  in  the  raphe. 

Abbreviations. — AS,  Aqueduct  of  Sylvius;  c.  Am.,  gyrus 
hippocampi;  cc,  corpus  callosum;  est,  nucl.  caudatus;  /, 
post.  long,  bundle;  firn,  fimbria;  li.  Is,  lateral  and  mesial 
fillets;  nam,  nucl.  amgydalse;  7iL  lenticular  nucleus;  nr, 
red  nucleus;  Putamen  teg,  thai,  fibers  to  the  optic  thala- 
mus; tro,  tractus  opticus;  u,  uncus;  vl,  v.  Ill,  lateral  and 
middle  ventricles. 


Tab.  40. 


Fixj.  1. 


Fig.  2. 


Tab.  41. 


^^^       v/F 


^* 


PLATE  41. 

Fig.  1. — Section  througJi  the  Tegmentum  behind  the  Poste- 
rior Corpora  Quadrigemlna  (behind  the  section  on  Plate 
38,  1).  The  aqueduct  is  just  beginning  to  widen  out  into 
the  fourth  ventricle  (r  IV). 

Note  the  structure  of  the  substantia  reticularis  (Srt), 
which  contains  descending  fibers  from  the  optic  thalami 
and  ascending  fibers  from  the  anterolateral  columns  of  the 
spinal  cord.  The  mesial  superior  fillet  (/>.  s,  main  fillet) 
subdivides  into  numerous  ])undles.  To  its  outer  side  is 
the  inferior  fillet  (L.  ?*),  part  of  which  ascends  to  the  poste- 
rior corpora  quadrigemlna.  Further  out  is  the  nucleus 
lateralis  (of  the  optic  thalamus). 

Brachia  (J5),  nasal  root  of  the  trigeminus  (  Fw),  poste- 
rior longitudinal  bundle  (/);  the  heavy  decussation  of 
fibers  in  the  raphe  (R)  of  the  tegmentum  is  plainly  seen 
(the  region  contains  central  sensory  and  motor  decussating 
pathways);  /.  c,  locus  coeruleus,  containing  deeply  pig- 
mented cells. 

Abbreviations. — P,  Pons;  Cb,  cerebellum;  v,  superior  ver- 
miform process. 

^  Fig.  2. — Section  through  the  Nuclei  of  the  Trigeminus  (in 
front  of  the  section  shown  on  Plate  48,  2).  Note  the 
details  of  the  tegmentum  and  of  the  nuclei  of  the  trigem- 
inus. The  caudal  descending  root  with  its  various  bundles 
(Vc)  is  very  plainly  seen  in  this  section  lying  between 
the  motor  (m)  and  sensory  (s)  nuclei.  Central  tegmental 
pathway  (ct),  substantia  reticularis  tegmenti  (Sr.  t),  pon- 
tine ganglia  (g)  between  the  superficial  (Ps)  and  deep 
(Pp)  pontine  fibers.  Tlie  raphe  of -the  tegmentum  (K) 
and  of  the  pontine  fibers  (R)  contains  numerous  decus- 
sating fiber  tracts.  Underneath  the  superior  olive  (o.  s) 
at  L.  i,  the  transverse  fibers  of  the  trapezoid  body  and 
inferior  fillet  (central  auditory  pathway)  are  seen. 

Abbreviations. — B,  Brachium;  Cb,  cerebellum;  Ic,  locus 
coeruleus;  N  V,  trigeminus  fibers;  Py,  pyramidal  tract; 
ma,  anterior  medullary  velum;  v,  vermis  sup.;  Nv,  nasal 
root  of  trigeminus. 


PLATE  42. 

Fig.  1. — Section  through  the  Bight  Tegmental  Region  at  the  Level  of  the 
Nucleus  of  the  Facial  Nerve.  Compare  this  figure  with  Plate  39, 1.  The 
fibers  of  the  nerve  ascend  singly  from  the  deeply  seated  nucleus 
(w.  VII). 

We  can  also  see  a  bundle  of  fibers  running  from  the  superior  olive 
{ol.  s)  to  the  nucleus  of  the  abducens  {N.  VI),  although  the  latter  is 
better  seen  in  more  anterior  sections.  Passing  down  from  the  cere- 
bellum we  see  the  restiform  body  ( Cr)  and  the  processus  cerebelli  ad 
pontem  (Cb). 

The  fibers  of  the  facial  {g.  VII )  unite  at  the  knee  to  form  the  nerve- 
trunk,  which  occupies  a  deeper  position  underneath  the  ependyma  of 
the  floor  of  the  fourth  ventricle  {v.  IV).  The  adjacent  ventral  nucleus 
of  the  auditory  nerve  is  joined  to  the  fillet  by  the  trapezoid  body 
(through  Li). 

On  the  outer  side  of  the  trunk  of  the  facial  lies  the  descending  root 
of  the  trigeminus  {V.  c) ;  immediately  in  front  of  it  is  the  substantia 
.gelatinosa  {S.  g),  which  represents  the  beginning  of  the  posterior  horn 
of  the  spinal  cord.  On  the  dorsal  side  we  find  the  dorsal  nucleus  of 
the  auditory  nerve  {n.  VIII),  and  Deiters'  nucleus  {N.  D),  with  the 
vestibular  nerve  {VIII  v),  which  enters  at  this  point;  superior  and 
inferior  fillets  (L.  s,  L.  i).  Substantia  reticularis  [Sr.  t);  central  teg- 
mental pathway  (c.  t);  raphe  {K);  pontine  ganglia  (g);  pontine 
fibers  (P). 

Fig.  2. — Section  through  the  Ventral  Nucleus  of  the  Auditory  Nerve  on 
the  Left  Side.  (Following  Plate  39,  2.)  The  restiform  body  (er)  has 
emerged  from  the  white  matter  of  the  cerebellum  and  forms  the  lateral 
wall  of  the  fourth  ventricle  {v.  IV).  To  its  lateral  side  is  the  semi- 
circular ventral  nucleus  of  the  eighth  nerve  (ri.  v.  VIII),  in  which  the 
cochlear  nerve  disappears.  The  nucleus  extends  some  distance  upward 
and  presents  a  large  transverse  section  as  high  up  as  the  level  shown  in 
Plate  39,  2.  Of  the  fibers  forming  the  central  pathway,  we  can  rec- 
ognize the  striae  acusticse  {str.  a),  which  cover  the  floor  of  the  fourth 
ventricle,  running  from  the  median  line.  They  decussate  in  the  raphe 
{K)  and  continue  their  cjourse  in  the  lateral  fillet.  Dorsal  nucleus  of 
the  eighth  nerve  {n.  VIII  d);  descending  root  of  the  eighth  {a.  d);  on 
the  mesial  side  the  nucleus  of  the  glossopharyngeal  {n.  IX);  the 
nucleus  of  the  facial  (w.  VII)',  the  substantia  reticularis  {Sr.  t);  the 
central  tract  of  the  tegmentum  (c.  t);  mesial  fillet  (L);  pyramid,  pos- 
terior longitudinal  bundle  (/);  and  flocculus  (fl)  ot  the  cerebellum. 

Vc,  descending  root  of  the  trigeminus.  At  fol  the  cerebello-olivary 
fibers  from  the  restiform  body  pass  down  through  the  nucleus  of  the 
lateral  column  situated  in  this  region.  Laterally  under  K,  nucleus 
reticularis  tegmenti;  /,  fasciculus  longitudinalis  posterior. 


Tab.  42. 


Fig.  1. 


Tab.  43. 


y'^-l-' 


Fig.  1. 


PLATE  43. 

Fig.  1. — Section  throuyh  the  Cerebellum  and  Medulla  Ob- 
longata (poaterior  portion  of  the  rhomboid  fossa).  The 
lateral  walls  of  the  fourth  ventricle  {v.  IV)  at  this  point 
are  formed  by  the  pia-arachnoid,  as  the  restiform  bodies 
(cr)  have  become  completely  separated  from  the  cerebellar 
hemispheres.  The  roof  of  the  ventricle  is  formed  by  the 
vermiform  process  (  F);  superior  {v.s)  and  inferior  vermi- 
form processes  {v.  i). 

In  the  cerebellum  we  see  the  corpus  dentatum  (c.  d)  and 
the  tegmental  nucleus  (n.  t).  The  cortex  of  the  hemi- 
spheres has  been  cut  away.     Nodulus  (n). 

In  the  medulla  we  see  the  pyramids  {Py)^  olives  (o/), 
restiform  bodies  (cr),  and  the  internal  arcuate  fibers  which 
leave  the  latter  structures  at  this  point. 

Fig.  2. — Section  through  the  Medulla  Oblongata  at  the  Level 
of  the  Glossopharyngeovagus  Nucleus.  By  the  side  of  the 
pyramids  (Py)  the  inferior  olives  (ol)  have  made  their 
appearance.  The  cerebellar  fibers  (/o/)  pass  out  from  the 
restiform  bodies  (cr)  to  the  olive  of  the  opposite  side. 
Between  the  olives  in  the  "  interolivary  layer  "  the  supe- 
rior fillet  (X)  is  seen  close  to  the  raphe  (K)»  Dor- 
sally  it  comes  into  relation  with  the  posterior  longitudinal 
bundle  (/).  The  space  between  the  latter  and  the  resti- 
form body  is  occupied  by  the  substantia  reticularis  (>S'.  r.  t) 
of  the  tegmentum,  while  on  the  dorsal  side  the  sensory 
nuclei  of  the  ninth  and  tenth  nerves  are  seen;  on  the  outer 
side  of  these  the  dorsal  nucleus  of  the  eighth  {n.  VIII d). 
In  front  of  the  restiform  body  is  the  descending  root  of  the 
ninth  and  tenth,  the  solitary  bundle  (8),  and  under  this 
the  descending  root  of  the  trigeminus  (  V.  c)  to  the  lateral 
side  of  the  substantia  gelatinosa  (S.g).  The  fibers  of  the 
ninth  and  tenth  emerge  on  the  surface  of  the  medulla  by 
the  side  of  the  solitary  bundle.  To  their  mesial  side  in 
the  tegmentum  is  a  group  of  cells  known  as  the  nucleus 
ambiguus  (n.  a),  or  motor  nucleus  of  the  vagus,  which  can 
also  be  seen  in  the  following  sections,  ol.  m,  Mesial  olive; 
ol.p,  posterior  accessory  olive;  Cb,  fibers  of  the  restiform 
body  belonging  to  the  direct  cerebellar  tract;  nf,  nucleus- 
arciformis,  surrounded  by  the  external  arcuate  fibers,  which 
emerge  at  the  raphe  and,  sweeping  over  the  pyramids,  join 
the  restiform  body. 


PLATE  44. 

Fig.  1. — Section  through  the  Medulla  at  the  Level  of  the 
Nuclei  of  the  Tenth  and  Twelfth  Nerves.  To  the  mesial  side 
of  the  nucleus  of  the  tenth  nerve  that  of  the  hypogiossus 
(XII)  makes  its  appearance  in  the  floor  of  the  fourth  ven- 
tricle. The  fibers  of  this  nerve  pass  upward  from  the 
posterior  longitudinal  bundle  (/)  and  fillet  (L).  To  the 
outer  side  of  the  olives  the  external  arcuate  fibers  (fac) 
pass  from  the  restiform  body  to  the  fillet  of  the  same  side, 
while  the  internal  arcuate  fibers  (fai)  pass  through  the 
substantia  reticularis  and  connect  the  fillet  with  the  mesial 
segment  of  the  restiform  body  of  the  other  side,  after 
traversing  the  descending  root  of  the  trigeminus  (Vc); 
hence  the}^  cross  in  the  raphe.  Above  the  inferior  olives 
(o/)  is  the  posterior  olive,  and  to  its  mesial  side  the  inter- 
nal or  accessory  olive  (ol.  m).  The  direct  cerebellar  tract 
(C6)  is  contained  in  the  restiform  body  and  continues 
downward  toward  the  pyramids,  fiol,  cerebello-olivary 
and  interolivary  fibers. 

Fig.  2. — Section  through  the  Calamus  Scriptorius  in  the 
Medulla.  The  restiform  bodies  {c.  r)  are  gradually  reduced 
in  size  as  more  and  more  fibers  are  given  off,  and,  ap- 
proaching each  other  in  the  median  line,  close  the  rhom- 
boid fossa  {v.  IV;  dorsally,  the  taenia  of  the  fourth  ven- 
tricle). The  nuclei  of  the  posterior  columns,  the  mesial 
nucleus,  or  nucleus  of  Goll,  and  lateral  nucleus,  or 
nucleus  of  Burdach  (71.  f.  p),  appear  in  the  restiform 
bodies.  From  these  nuclei  the  internal  arcuate  fibers 
(fai)  descend  in  massive  bundles  to  the  fillet  (L)  of  the 
other  side.  The  nucleus  of  the  hypogiossus  (ri.  XII)  and 
the  central  canal  (cc)  occupy  a  deeper  position.  Termin- 
ation of  the  nucleus  of  the  tenth. 

Pr,  Pyramids;  L,  fillet;  Srt,  substantia  reticularis;  S.  g, 
substantia  gelatinosa;  V.  c,  descending  root  of  the  trigem- 
inus; Cb,  direct  cerebellar  tract;  s,  solitary  bundle;  ol, 
olives;  /,  posterior  longitudinal  bundle,  etc.,  as  in  former 
plates.  K,  raphe  of  the  tegmentum;  fac,  external  arcuate 
fibers. 


Tab.  44. 


-^'J 


]  Fig.  2. 


Tab.  45. 


PLATE  45. 

Fig.  1. — Section  through  the  Nuclei  in  the  Posterior  Columns. 
Above  the  nuclei  of  GoU  (n.  G)  and  Burdach  (n.  B)  the 
corresponding  funiculi  (gracilis  and  cuneatus)  are  plainly 
seen  sharply  separated  from  each  other.  The  central 
canal,  and  with  it  the  nucleus  of  the  hypoglossus  (XII), 
have  descended  further  into  the  substance  of  the  medulla. 
The  internal  (fai)  and  external  (fae)  arcuate  fibers  are 
plainly  visible.  Everything  else  as  in  the  preceding  sec- 
tions, except  that  the  olives  (ol)  are  considerably  dimin- 
ished in  size.  Ca,  beginning  of  the  anterior  horn  of  the 
spinal  cord;  Sg,  beginning  of  the  posterior  horn. 

Fig.  2. — Section  through  the  Medulla  below  the  Olives. 
After  the  olives  have  disappeared,  the  medulla  becomes 
considerably  smaller.  The  nuclei  of  GoU  (n.  G)  and  Bur- 
dacli  (n.  B)  are  smaller,  while  the  corresponding  funiculi 
(gracilis  and  cuneatus)  are  larger.  The  nucleus  of  the 
hypoglossus  has  disappeared,  and  that  of  the  spinal  acces- 
sory makes  its  appearance  in  the  anterior  horn  (Ca). 

The  area  occupied  by  the  direct  cerebellar  tract  is  clearly 
outlined,  and  is  joined  on  its  dorsal  side  by  the  substantia 
gelatinosa  (S.  g),  on  the  outer  side  of  which  w^e  see  the 
descending  root  of  the  trigeminus  (  F.  c).  fai  and  fae,  inter- 
nal and  external  arcuate  fibers;  S.  rt,  substantia  reticularis; 
L,  fillet  (considerably  reduced  in  size);  K,  decussation  of 
the  fillet;  Py,  pyramids;  olm,  internal  secondary  olive  as 
on  Plate  44.  Between  the  colunms  of  GoU  the  posterior 
longitudinal  sulcus  (*S'.  p),  and  between  the  pyramids  the 
anterior  longitudinal  sulcus  (S.a).  In  the  pyramids  the 
arciform  nucleus  (n.  a). 


PLATE  46. 

Fig.  1. — Section  Immediately  above  the  Decussation  of  the 
Pyramids.  The  pyramids  (Py)  occupy  a  deeper  position 
and  tend  to  approach  each  other,  thus  separating  the  nar- 
row layer  of  the  fillet  (fa)  into  two  portions.  The  poste- 
rior longitudinal  bundle  (/)  is  still  visible  at  the  summit 
of  the  pyramids.  The  internal  arcuate  fibers  (fai)  are 
plainly  seen  emerging  from  the  nucleus  of  Goll  {n.  G)  to 
pass  to  the  fillet  of  the  opposite  side  (decussation  of  the 
fillet). 

The  nuclei  of  the  posterior  columns  (a.  G.  and  B.)  have 
diminished,  while  the  substantia  gelatinosa  (aS'.  g)  has  be- 
come more  massive  (beginning  of  the  posterior  horn, 
corn.  p).  In  the  substantia  reticularis  tegmenti  (6V^)  the 
region  between  the  remains  of  the  fillet  and  longitudinal 
bundle  corresponds  to  the  beginning  of  the  anterior  horn 
(corn.  a).  The  fibers  of  the  sul)stantia  reticularis  on  the 
outer  side  of  the  anterior  horn,  the  anterolateral  ground 
bundle  (/),  and  Gowers'  tract  (G),  the  direct  cerebellar 
tract  (CI)  being  situated  more  posteriorly.  In  the  middle 
we  see  the  nucleus  of  the  twelfth  nerve,  which  disappears 
at  this  point.  The  accessory  olives  have  disappeared. 
The  spinal  portion  of  the  eleventh  nerve  arises  in  cells 
situated  in  the  lateral  portion  of  the  anterior  horn.  For 
the  remaining  letters  see  Plate  45. 

Fig.  2. — Section  through  the  Decussation  of  the  Pyramids. 
The  nuclei  of  the  posterior  columns  have  disappeared, 
and  the  posterior  segment  is  entirely  occupied  by  the  pos- 
terior colunms  (column  of  Goll  and  colunm  of  Burdach, 
/.  G.  B). 

The  pyramids,  after  undergoing  decussation,  traverse 
the  substance  of  the  anterior  horn  (D.  Py)  and  enter  the 
lateral  column  of  the  other  side;  the  decussation  of  the 
fillet  has  disappeared.  The  posterior  horn  (S.  g)  is  plainly 
seen.  The  other  structures  are  the  same  as  in  the  preced- 
ing cut. 

C.a,  Anterior  horn;  c.c,  central  canal;  S.a,  posterior  sul- 
cus; fal,  lateral  column;  N  XI,  spinal  accessory  nerve 
emerging  at  the  lateral  surface  of  the  cord.  Its  nucleus  is 
situated,  in  the  anterior  horn  (Ca);  ra,  highest  anterior 
root  of  the  first  cervical  nerve. 


Tab.  46. 


Fig.  1. 


MV/ 


Tab.  47. 


Sol    - 


Fig. 


PLATE  47. 

Beginning  with  this  plate  the  sections  are  shown  inverted,  accord- 
ing to  the  usual  custom.  The  dorsal  segment  {S. p)  is  below;  the  ven- 
tral [S.  a),  above. 

Fig.  1. — Section  through  the  Spinal  Cord  immediately  be- 
low the  Decussation  of  the  Pyramids.  The  pyramids  (Py) 
have  for  the  most  part  disappeared  from  the  anterior  col- 
umn, and  are  now  contained  in  the  lateral  column  of  the 
other  side.  The  anterior  column  now  contains  the  un- 
crossed pyramidal  tract  {Py.  a)  and  the  anterior  ground 
bundle  (fa),  consisting  partly  of  the  posterior  longitudi- 
nal bundle.  The  lateral  column  contains  the  crossed  or 
lateral  pyramidal  tract  (Py);  the  anterolateral  ground 
bundle  (fal)  and  Gowers'  tract  (G)  being  the  continuation 
of  the  fibers  of  the  substantia  reticularis  tegmenti;  the 
direct  cerebellar  tract  (C.  6),  consisting  of  the  restiform 
bodies  (ventral  portion).  The  posterior  columns  contain 
the  column  of  Goll  (/.  G)  and  the  column  of  Burdach 
(f.B). 

At  the  bottom  of  the  anterior  longitudinal  sulcus  (S.a) 
we  see  the  anterior  commissure  (d),  the  spinal  continua- 
tion of  the  decussation  of  the  pyramids,  and  dorsally  the 
central  canal  (c.  c)  and  the  posterior  commissure. 

The  anterior  horn  (C.  a)  and  tlie  posterior  horn  (c.  p) 
are  now  fully  formed.  In  the  posterior  horn  the  substan- 
tia gelatinosa  (♦S'.  g),  which  is  visible  in  higher  sections,  is 
still  very  well  represented.  The  roots  of  the  highest  cer- 
vical nerves  here  emerge  from  the  anterior  horn  (anterior 
roots),  and  the  posterior  fibers  enter  the  lateral  portion  of 
the  column  of  Burdach  (the  posterior  roots  enter  the  pos- 
terior root-zone). 

Fig.  2. — Section  through  the  Spinal  Cord,  at  the  Level  of 
the  Fourth  Cervical  Nerve.  Lettering  as  in  Figure  1.  The 
substantia  gelatinosa -(c.  p)  in  the  posterior  horn  is  now 
much  reduced  in  size  and  appears  smaller  and  smaller  in 
succeeding  sections.  Origin  of  the  phrenic  nerve  in  the 
cells  of  the  anterior  horn  (Ca).    rp.  Posterior  roots. 


PLATE  48. 

Fig.  1. — Section  through  the  Cervical  Enlargement  at  the 
Level  of  the  Seventh  Cervical  Nerve  (Plexus  Brachialis).  Owing 
to  the  vigorous  development  of  the  gray  matter,  the  an- 
terior horn  (C  a)  has  materially  increased  in  width.  The 
arrangement  of  the  structures  is  the  same  as  in  Plate  47, 
Figure  1.  The  anterior  horn  contains  the  cells  for  the 
motor  peripheral  neurons  for  the  muscles  of  the  arm  at 
this  level,  especially  of  the  muscles  of  the  forearm.  The 
ganglion  cells  are  divided  into  a  small  mesial  (m),  and  a 
lateral  (7)  group.  The  lateral  and  mesial  groups  are  again 
subdivided  into  anterior  (I.  a)  and  posterior  (/.  ]>)  segments. 
It  is  probable  that  the  true  motor  ganglion  cells  are  sit- 
uated in  the  lateral  groups.  Behind  the  motor-cell  groups 
are  the  so-called  ''  middle  cells  "  (c),  which  are  surrounded 
by  the  terminal  fil)rils  of  numerous  collaterals  from  the 
posterior  roots  and  from  the  lateral  columns.  The  poste- 
rior roots  (?\  p)  and  their  course  can  be  studied  better  on 
Plate  52,  Figure  1. 

Fig.  2. — Section  through  the  Thoracic  Portion  of  the  Spinal 
Cord  at  the  Level  of  the  Third  Thoracic  Nerve. 

Fig.  3. — Section  through  the  Thoracic  Portion  of  the  Cord 
at  the  Level  of  tJie  Sixth  Thoracic  Nerve.  The  peripheral 
neurons  for  the  intercostal  muscles  emerge  from  the  ante- 
rior horn,  which  is  narrower  at  this  point  than  in  the  cer- 
vical enlargements.  At  the  base  of  the  posterior  horn  the 
first  indications  of  the  columns  of  Clarke  (CI)  are  seen. 
cc,  Central  canal. 

The  columns  of  Goll  gradually  disa})pear  as  we  go  fur- 
ther down  the  cord.  The  relations  of  other  structures  are 
the  same.     r.  a,  Anterior  roots;  r.  p^  posterior  roots. 

Abbreviations. — Ca,  Anterior  horn;  ca,  anterior  commis- 
sure; Cb,  direct  cerebelhir  tract;  cr,  central  canal;  cl,  col- 
umns of  Clarke;  cp,  posterior  horn;  fa,  anterior  column 
(ground  bundle);  fal,  lateral  column  (ground  bundle); 
fB,  fG,  columns  of  Burdach  and  Goll;  G,  Gowers'  tract; 
X,  boundary  zone  of  Lissauer;  ra,  rp,  anterior  and  posterior 
roots;  Sa,  Sp,  anterior  and  posterior  longitudinal  sulcus; 
Py,  lateral  pyramidal  tract;  Pya,  anterior  pyramidal  tract. 


Tab.  48. 


Fig.  1. 


Tab.  49.. 


C^^„   Sa 


Fig.  1. 


J^Wf^ ^»^-^r^.Sa, 


Fig.  2. 


Fig.  3. 


PLATE  49. 

Fig.  I. — Section  through  the  Thoracic  Portion  of  the  Cord 
at  the  Level  of  the  Eleventh  C&rvical  Nerve.  Tiie  anterior 
horn  {C.a)  again  increases  in  size  and  its  contour  is 
altered.  The  cells  of  the  columns  of  Clarke  {C.l)  have 
become  larger  and  are  quite  conspicuous.  Fibers  from 
these  cells  enter  the  direct  cerebellar  tract  (C6,  Plate  48) 
of  the  same  side,  and  pass  by  way  of  the  restiform  bodies 
to  the  tegmental  nucleus  of  the  opposite  side  in  the  cere- 
bellum. Below  the  origin  of  the  direct  cerebellar  tract  the 
lateral  pyramidal  tract  {Py)  appears  at  the  periphery  of 
the  cord.  The  anterior  pyramidal  tract  becomes  smaller 
and  smaller  and  is  gradually  lost  in  the  upper  portion  of 
the  lumbar  cord;  the  remaining  columns  of  the  cord  are 
similarly  decreased  in  size,  having  given  off  a  portion  of 
their  fibers  at  higher  levels. 

Fig.  2. — Section  through  the  Upper  Portion  of  the  Lumbar 
Cord  at  the  Level  of  the  Second  Lumbar  Nerve. 

Fig.  3. — Section  through  the  Lower  Portion  of  the  Lumbar 
Cord  at  the  Level  of  the  Fourth  Lumbar  Nerve.  The  anterior 
and  posterior  horns  appear  very  massive;  the  gray  matter 
is  almost  in  excess  of  the  white  matter.  The  cell-groups 
in  the  anterior  horn,  like  their  homologues  in  the  cervical 
enlargement,  are  divided  into  a  mesial  group  (anterior 
and  posterior,  ga)  and  very  much  larger  anterior  (la)  and 
posterior  (Ip)  lateral  groups,  c,  Intermediate  zone.  The 
peripheral  neurons  for  the  muscles  of  the  leg  are  given 
off  from  the  lateral  group.  The  posterior  roots  (r.p)  are 
collected  into  massive  bundles  and  enter  the  posterior 
root-zones;  their  collaterals  and  shorter  branches  (radii) 
arch  backward  into  the  posterior  horn.  Sg,  substantia 
gelatinosa  in  the  posterior  horn ;  B,  column  of  Burdach. 
For  remaining  letters  see  Plate  48. 


PLATE  50. 

Pig.  1. — Section  through  the  Middle  Sacral  Portion  of  the 
Cord  at  the  Level  of  the  Third  Sacral  Nerve.  The  termina- 
tion of  the  lateral  pyramidal  tract  (Py)  is  seen  in  the 
white  substance  of  the  lateral  column.  The  gray  matter 
is  relatively  greatest  at  this  level.  The  broad  anterior 
horn  (Ca)  contains  the  motor  ganglion  cells  of  the  per- 
ipheral neuron  for  the  small  muscles  of  the  feet,  and,  at 
a  somewhat  deeper  level,  those  for  the  anal  and  vesical 
muscles  and  for  the  fibers  which  subserve  the  reflex  and 
automatic  activity  of  these  organs,  i?,  Column  of  Bur- 
dach;  ^S'^',  substantia  gelatinosa  of  the  posterior  horn. 

Fig.  2. — Section  through  the  Cauda  Equina  and  the 
Conus  Medullaris.  Lying  within  the  dural  sac  are  the 
motor  and  sensory  roots  for  the  nerves  of  the  lower  ex- 
tremity, which  emerge  from  the  cord  at  a  higher  level  and 
continue  for  some  distance  within  the  vertebral  canal;  the 
constituents  of  the  crural  nerve  (PL  I)  in  the  lateral, 
those  of  the  sciatic  (PI.  s)  in  the  mesial,  portion.  The 
former,  after  their  exit  from  the  cord,  form  the  lumbar, 
the  latter  the  sacral,  plexus.  In  the  center  of  the  figure 
we  see  the  conus  medullaris  (C.  m),  which  forms  the 
tip  of  the  spinal  cord. 

Fig.  3. — Section  through  the  Posterior  Root  and  Spinal 
Ganglion  from  the  Lumbar  Portion  of  the  Cord.  The  mixed 
nerve  (N.p)  coming  from  the  periphery  divides  at  the  dis- 
tal boundary  of  the  ganglion,  its  sensory  portion  (r.a) 
entering  the  ganglion  and  terminating  in  its  cells.  Al- 
though the  magnification  is  low,  a  portion  of  the  darkly 
pigmented  cells  of  the  ganglion  can  be  made  out.  The 
fibers  from  these  cells  collect  into  a  bundle  and  form  the 
posterior  root  (r.p),  which  enters  the  spinal  cord,  espe- 
cially the  posterior  root-zone  in  the  posterior  column,  fa, 
Afferent,  fe,  efferent,  fibers;  c,  cells  of  the  ganglion. 


Tab.  50. 


Fig.  1. 


Fig.  2. 


Fig.  3. 


Tab.  51. 


m^m^ 


'     Fig.l. 


Fig.  2. 


Fw.^. 


Fig,  3. 


PLATE  51. 

Fig.  1.  —  Transverse  Section  through  the  Entire  Sciatic  Nerve 
at  its  Point  of  Exit  {Great  Sciatic  Eorameu;).  With  a  lower 
power  the  numerous  hundles  (/)  of  different  sizes  which 
make  up  the  nerve  are  plainly  seen,  surrounded  by  the 
epineurium  (P).  The  blood-vessels  are  seen  among  the 
cells  in  the  perineural  connective  tissue. 

Fig.  2. — Longitudinal  Section  of  a  Nerve  Bundle  from  the 
Sciatic  Nerve.     For  further  description  see  Figure  3. 

Fig.  3. — Transverse  Section  of  a  Nerve  Bundle  from  the 
Sciatic  Nerve.  With  a  higher  power  it  appears  that  the 
bundle  is  composed  of  medullated  fibers  (black)  of  vary- 
ing sizes.  In  the  various  nerve  bundles  numerous  very 
delicate  nerve-fibers  with  barely  perceptible  medullary 
sheaths  are  seen  scattered  without  any  apparent  order 
among  the  fibers  of  the  largest  caliber.  The  nerve 
bundle  is  subdivided  into  separate  compartments  by  the 
endoneural  connective  tissue. 

Fig.  4. — Transverse  Section  of  a  Normal  Optic  Nerve  and 
Sheath  (low  power).  This  nerve  also  consists  of  numerous 
bundles  which  contain  the  minute  nerve-fibers.  The  optic 
nerve  contains  more  than  400,000  individual  fibers. 


PLATE  52. 
The  Gray  Matter  of  the  Spinal  Cord. 

The  two  photographs  present  the  right  half  of  a  section 
through  the  cervical  portion,  and  the  left  half  of  a  section 
through  the  lumhar  portion  of  the  cord  under  high  power. 
For  the  lettering  see  Plate  48,  Figure  1,  and  Plate  39, 
Figure  3. 

Note  especially  the  vast  number  of  fibers  which  enter 
into  and  emerge  from  the  horns.  The  anterior  horn 
receives : 

1.  Fibers  from  the  anterior  commissure  (decussating 
fibers  from  the  anterior  pyramidal  tract  and  decussating 
central  sensory  fibers). 

2.  Fibers  from  the  anterolateral  column  (t(a-minal 
motor  fibers,  collaterals  from  the  lateral  pyramidal  tract, 
and  sensory  central  collaterals  from  the  anterolateral  tract). 

3.  Fibers  from  the  posterior  horn  (reflex  collaterals 
and  other  posterior  root-fibers)  which  pass  to  the  middle 
zone  and  to  the  anterior  horn. 

From  the  anterior  horn  emerge  the  anterior  motor  roots 
(rrt),  which  arise  from  the  groups  of  motor  ganglion  cells 
and  emerge  in  bundles  at  the  surface  of  the  anterolateral 
column.  They  are  derived  principally  from  the  lateral 
cell  groups. 

The  posterior  horn  receives  from  the  posterior  column 
massive  arching  bundles  (r)  containing  the  collaterals  and 
all  the  short  tracts  of  the  posterior  roots  (rp).  The  sub- 
stantia gelatinosa  (S.  g),  situated  at  the  posterior  extremity 
of  the  posterior  horns,  is  capped  by  the  boundar}^  zone  of 
Lissauer  (L),  consisting  of  delicate  posterior  root-fibers, 
and  immediately  in  front  of  Lissauer' s  zones  we  see  the 
zona  spongiosa  of  the  posterior  horns.      (See  Plate  26. ) 


Tab.  53. 


Fig. 


Fig.  J,. 


Fig.n 


Fig.  6. 


Fig.  7. 


PLATE  53. 
Process  of  Medullation  in  the  Fetal  Brain.     (Photographs.) 

This  plate  belongs  immediately  after  Plate  15. 
been  introduced  at  this  point  for  the  sake  of  greater  clearness. 

Figures  1  to  5  represent  sections  through  the  unstained  brain-stem 
of  an  eight  months'  fetus,  Nearly  all  the  fibers  which  in  the  fully 
formed  brain  are  medullated — that  is  to  say,  white  when  unstained — 
appear  nonmedullated  in  these  sections.  On  the  other  hand,  certain 
important  tracts,  which  are  evidently  quite  old  in  a  genetic  sense, 
can  be  readily  picked  out  even  with  the  naked  eye  by  the  presence  of 
the  nerve  sheath,  their  glistening  white  color  contrasting  with  the 
gray  of  the  remaining  brain-stem.  The  most  important  of  these  path- 
ways are:  The  radiation  to  the  red  nucleus  (h.  r)  (Fig,  1,  L),  the  ansa 
lenticularis  {cL),  and  the  fillet  {Ls.  i).  In  addition  to  these,  the  pos- 
terior longitudinal  bundle  (/),  the  brachia  (6),  the  nasal  trigeminus 
root,  the  peripheral  cranial  nerves,  the  optic  tract  [tro],  the  posterior 
commissure  (cj)),  are  medullated.  The  pyramidal  tract  has  not  yet 
become  medullated. 

Figs.  1  and  2. — Section  through  the  Middle  and  Posterior  Segments  of 
the  Optic  Thalamus.  Note  the  crusta  (motor  pyramidal  tract,  etc,), 
which  has  not  yet  become  medullated. 

Fig,  3. — Section  through  the  Anterior  Corpora  Quadrigemina. 

Fig,  4, — Section  through  the  Middle  of  the  Pons. 

Fig.  5. — Section  through  the  Medulla  Oblongata.  Bundles  of  fibers 
which  early  become  medullated  ascend  from  the  region  of  the  fillet 
above  the  levels  shown  in  section  1,  and  after  joining  the  ansa  lenticu- 
laris and  traversing  the  globus  pallidus  (probably  without  interrup- 
tion), enter  the  so-called  tegmental  radiation  (the  earliest  medullated 
fiber  tract  of  the  cerebral  medulla,  sensory  path  way ;  see  text,  Part  IV), 
to  end  in  the  cortex  of  the  posterior  central  convolution  and  of  the 
parietal  lobe. 

Figs,  6  and  7. — Sections  through  the  Cervical  and  Thoracic  Portions 
of  the  Spinal  Cord  from  a  New-born  Infant.  The  pyramidal  tract  (Py), 
which  is  not  medullated,  is  readily  distinguished  from  the  fully  devel- 
oped direct  cerebellar  tract  {Cb).  (For  the  corresponding  segment  of 
the  spinal  cord  see  Plate  14,  Fig.  2 — medullary  sheath  stain, ) 


PLATE  54. 

Schema  of  the  Most  Important  Nerve  Tracts  from  a  Clinical 
Point  of  View. 

The  following  pathways  and  their  relative  position  in 
both  halves  of  the  cord  are  indicated  in  the  transverse  sec- 
tions of  the  cerebral  hemispheres,  crura,  pons,  cerebellum, 
medulla  oblongata,  cervical  and  lumbar  enlargement. 

1.  Motor  Pathway. — Central  neuron  complex  (pyramidal 
tract),  red;  peripheral,  blue.  Note  the  decussations  of  the 
central  pathways  (d  VII,  d  XII,  dp,  decussations  of  the 
facial  and  hypoglossus  fibers  and  of  the  pyramids). 

Abbreviations. — Py,  Pyramidal  tract;  Pya,  Pyl,  anterior 
and  lateral  pyramidal  tracts. 

2.  Sensory  Pathway. — Peripheral  neuron,  brown;  central 
(tract  of  the  fillet),  green;  centrocortical,  yellow. 

Abbreviations. — Cb,  Direct  cerebellar  tract;  Cr,  restiform 
body;  c  trap,  trapezoid  body;  LI,  Ira,  lateral  and  mesial 
fillel;  L,  superior  fillet;  c.^,  subthalamic  body. 

3.  The  pathway  uniting  the  red  nucleus  (nucl.  ruber) 
with  the  cer(il^ellum  (brachium,  b,  and  corpus  dentatum, 
cd)  is  colored  brown. 

4.  The  cerebello-olivary  tracts  are  yellow.  The  rest 
explains  itself. 


Tab.  J4. 


Ltth.  Anst  F.  Rdrhhxtld,  Miiiuiien . 


Tab.  oS. 


Iig.l. 


Fig.3. 


LUh.  Anst  t:  Keichhold.  Miinchen . 


PLATE  55. 

Figures  1  and  2  show  the  manner  in  which  the  tegmen- 
tum and  crusta  are  formed  from  the  tracts  of  the  cerebral 
hemispheres. 

Figure  1  shows  the  hemisphere  in  frontal  section;  Fig- 
ure 2,  in  a  horizontal  section. 

The  left  side  of  Figure  1  shows  the  formation  of  the 
crusta,  the  right  side  that  of  the  tegmentum. 

Crusta:  Frontal  pontine  tract  (dotted  blue  line);  pyr- 
amidal tract  (red) ;  temporo-occipital  pontine  tract  (l3lue). 

Tegmentum:  Tract  of  the  fillet  (blue);  optic  thalamus 
— red  nucleus — (brown);  ansa  lenticularis  (green). 

The  sections  of  the  hemispheres  show  diagrammatic- 
ally:  The  short  and  long  association  tracts  (brown);  the 
fibers  of  the  corona  radiata  running  to  the  optic  thalamus 
— upper  and  lower  peduncles — (brown). 

Figure  2  shows  in  addition  the  optic  radiation — occipi- 
tal cortex,  optic  centers,  optic  tracts  (yellow). 

Fig.  3. — Schema  of  the  Optic  Nerve  and  the  Oculomotor 
Tract  with  their  Connections  {the  Fibers  of  the  Left  Optic  Tract 
are  colored).  Optic  nerve:  peripheral  neuron  (brown),  in 
the  retina  (6,  bulbus);  central  neuron  (green),  in  the  optic 
nerve  (?!.  II)  as  far  as  the  chiasm  {Ch)  (decussation  of 
the  nasal  bundles),  thence  to  the  optic  tract  {tr.  o),  to  the 
lateral  geniculate  body  (cgl),  pulvinar  (7V<),  and  to  the 
anterior  corpus  quadrigeminum  (cqa),  where  the  tract 
breaks  up  into  terminal  fibrils.  From  this  point  the  path- 
way follows  the  optic  radiation  (yellow,  green)  to  the 
cuneus  in  the  occipital  lobe  (it  is  doubtful  whether  fibers 
pass  directly  from  the  tracts  to  the  cortex)  (collaterals?). 

Oculomotor:  Centred  neuron  (red),  from  the  cortical  cen- 
ter (g.,  angularis?),  containing  both  crossed  and  uncrossed 
fibers  to  the  nucleus  of  the  oculomotor  nerve  in  the  floor 
of  the  aqueduct. 

Peripheral  neuron  (blue)  :  From  this  point  as  peripheral 
neuron  to  the  muscles  of  the  eyeball  (fibers  also  originate 
on  the  opposite  side  for  the  internal  rectus). 

Pupillary  reflex  arc:  Fibers  of  the  oj^tic  nerve — corpora 
quadrigemina,  hypothetical  reflex  collaterals  (dotted  yel- 
low line),  nucleus  of  oculomotor,  peripheral  nerve  (blue), 
sj)hincter  pupillse  (the  ciliary  ganglion  is  interposed). 


PLATE  56. 

Fig.  1. — General  View  of  the  Projection  Paths.  Tlie  pro- 
jection paths  which  connect  deeper  portions  of  the  brain 
Avith  the  cortex,  after  leaving  the  cerebral  cortex  unite  to 
form  the  corona  radiata  and  enter  the  internal  capsule. 
Thence  some  of  the  fibers  forming  the  corona  radiata  enter 
the  optic  thalamus  (brown)  (anterior,  posterior,  superior, 
inferior  peduncles).  The  frontal  and  temporal  pontine 
pathway,  which  reaches  the  cerebellum  through  the  middle 
cerebellar  peduncle  of  the  other  side,  is  colored  blue. 
The  pyramidal  tract  is  red,  the  sensory  tract  of  the  fillet 
green,  the  cerebello-olivary  tract  violet,  the  optic  radiation 
yellow,  the  brachia  brown. 

Fig.  2. — Schema  of  the  Position  of  the  Sensory  Nerve  Tracts. 
The  peripheral  sensory  neuron  is  brown,  the  centrocortical 
green.  The  arrangement  of  the  cells,  the  course  of  the 
fibers,  their  manner  of  termination,  the  collaterals,  reflex 
arcs,  etc. ,  are  readily  seen  in  the  figure. 

/,  Olfactory  pathway;  //,  visual  pathway;  VIII,  audi- 
tory pathw^ay;  F,  IX\  gustatory  pathway  or  pathway  of 
cutaneous  sensation. 


Tab.  S6\ 


6.  Hippocampi         g. occipitalis        g.  temporal,  sup. 


gyn     central,      et    parietales 
LUJi.  Afial  t'.  ReidilwUl,  Munrhen . 


Tab.  SZ 


LUh..  Anst  t:  ReichholdyMiuifhen . 


PLATE  57. 
Schema  Showing  the  Course  of  the  Fibers  in  the  Spinal  Cord. 

I.  Motor  Pathway. 

(a)  Central  neuron  (red):  Lateral  pyramidal  tract  (Py.I)  and  ante- 
rior pyramidal  tract  {Py.a)]  terminal  fibrils  in  the  anterior  horn  (e«). 

(6)  Peripheral  neuron  (blue):  Cell  in  anterior  horn,  anterior  root 
{r.a),  motor  nerve  mnscle. 

II.  Sensory  Pathway. 

(«)  Peripheral  neuron  (brown):  sensory  nerve  {N.p)^  spinal  gan- 
glion ( Sp)  , posterior  root  ( r.p )  of  the  spinal  cord.  In  the  posterior  root- 
zone  of  the  posterior  cord  each  fiber  divides  into  an  ascending  and  a 
descending  branch  ( short  and  long  fibers) .  The  short  tracts  are  reflected 
into  the  posterior  horn  [ep)  and  consist  of:  (1 1  Reflex  collaterals  going 
to  the  anterior  horn,  short  reflex  arc,  long  reflex  arc.  (A  green  neuron 
is  interposed.)  (2)  Fibers  running  to  the  cells  in  the  middle  zone  of 
the  gray  matter.  (3)  Filjers  running  to  the  cells  of  the  columns  of 
Clarke  (c).  (4)  Fibers  running  to  the  central,  and  especially  to  the 
mesial  cells  in  the  anterior  horn  (commissural  cells).  (5)  Fibers  run- 
ning to  cells  in  the  posterior  horn. 

The  long  tracts  (6)  fii*st  enter  the  columns  of  Burdach  iB),  and 
higher  up  the  columns  of  Goll  (6r),  and  pass  to  the  funiculus  gracilis 
and  funiculus  cuneatus  in  the  medulla  oblongata  (at  this  point  the 
fillet  begins). 

(6)  Central  neuron  (green):  Its  beginning  corresponds  to  the  cells 
named  under  2  to  6,  where  the  peripheral  neuron  ends. 

1.  From  the  cells  mentioned  under  a  ("Strangzellen  ")  arise  the 
fibers  of  the  anterolateral  ground  bundle  {fal)  and  (fa.)  of  the  same 
side  (ground  bundle  of  the  anterolateral  columns »,  and  tho.se  of  Gowers' 
tract  [G). 

2.  From  the  cells  under  3:  The  direct  cerebellar  tract  {Ch)  of  the 
same  side. 

3.  From  the  cells  under  4:  Fibers  which,  after  decussating  in  the 
anterior  commissure,  ascend  in  the  anterolateral  column  {fa)  of  the- 
other  side. 

4.  From  the  cells  under  5:  Fibers  running  to  the  lateral  ground 
bundle  (  H)  and  to  the  ventral  field  of  the  posterior  columns.  (See 
Plate  26,1.) 

The  figures  also  show  the  manner  in  which  the  collaterals  are  given 
ofiE  and  the  termination  of  the  central  short  tracts  of  the  anterolateral 
column  (which  soon  reenter  the  gray  matter)  in  the  internal  cells 
("  Binnenzellen  "),  colored  green  (Golgi),  in  the  posterior  horn.  The 
decussation  which  takes  place  in  the  posterior  commissure  is  not  per- 
fectly understood  as  yet.  It  appears  that  the  posterior  roots  also 
contain  a  few  scattered  centrifugal  fibers  which  have  their  neuron  cells 
in  the  anterior  horn,  but  their  existence  in  man  has  not  as  yet  been 
definitely  established. 


IV. 
GENERAL    PATHOLOGIC   ANATOMY 

OF  THE 

NERVOUS  SYSTEM. 

ILLUSTRATED  BY  INDIVIDUAL  EXAMPLES. 

(Part  IV.  of  Text.) 


SPECIAL   PATHOLOGY    OF    THE    BRAIN. 

(Part  V.  of  Text.) 

Secondary  Diseases  of  the   Nervous  System. 


PLATE  58. 

Fig.  1. — Section  through  the  Cerebral  Cortex  and  Meninges 
in  Epidemic  Cerebrospinal  Meningitis.  Tlie  preparation  is 
taken  from  a  soldier  aged  twenty-three,  who  was  suddenly 
taken  ill  with  general  febrile  symptoms,  vomiting  and 
headache,  and  pain  and  rigidity  in  the  back  of  the  neck. 
Continuous  fever  ranging  about  104°  F.;  herpes  labialis; 
the  diagnosis  was  confirmed  by  a  leukocytosis  of  36,000. 
The  mental  condition  gradually  became  worse,  motor  irri- 
tative phenomena  (twitching  of  the  muscles  of  the  face 
and  of  the  arms,  especially  on  the  right  side)  and  delirium 
made  their  appearance.  The  patient  died  after  six  days 
in  deep  coma,  with  marked  persistent  rigidity  of  the 
nuchal  and  dorsal  nmscles. 

Autopsy. — Purulent  infiltrations  in  and  upon  the  soft 
membranes  of  the  brain  and  spinal  cord,  especially  over 
the  convexity  of  the  hemispheres,  and  most  marked  about 
the  middle  of  the  left  central  convolutions.  The  pus  con- 
tained the  diplococcus  lanceolatus.  The  purulent  infiltra- 
tion (colored  red)  dips  down  into  the  fissures  and  accom- 
panies the  pial  vessels  into  the  cortical  substance.  The 
effect  of  the  inflammatory  products  on  the  cortical  cells  is 
to  throw  them  at  first  into  a  morbid  state  of  irritation  and 
later  to  abolish  their  activity. 

Fig.  2. — Cerebral  Cortex  in  Tubercular  Meningitis.  In  a 
woman  thirty  years  old  in  an  advanced  stage  of  pulmo- 
nary tuberculosis  the  following  symptoms  appeared  twenty 
days  before  death:  Rise  in  the  fever-curve,  headaches,  de- 
lirium, increasing  coma,  ptosis  of  the  eyelids,  dilatation 
of  the  pupil,  convulsions. 

Diagnosis.  — Miliary  tuberculosis. 

Autopsy. — Small  grayish-white  nodules  are  scattered 
over  the  soft  membranes.  The  base  is  covered  with  a 
gelatinous  exudate  containing  tubercles,  in  w^hich  the 
oculomotor  nerve  is  embedded.  The  preparation  shows 
one  of  these  miliary  tubercles  taken  from  the  bottom  of  a 
sulcus;  the  growth  of  the  tubercle  has  gradually  en- 
croached on  the  cell-layer  of  the  cortex.  These  solitary 
tubercles  are  apt  to  increase  in  size,  especially  in  children, 
until  they  form  large  tumors.  (See  Plate  62. )  In  this 
case  we  have  a  disseminated  form  of  tuberculosis. 


Tub.  .7,9. 


3^, 


Mg.l. 


Eiy.S. 


JMh.  Anst.  F.  Reichhald.  Miwrhen. 


:^ 


Tah.  59. 


Lith.  Anst  E  KeutihoUl,  Miinrheu . 


PLATE  59. 

Fig.  1. — An  aneurysm  (An)  situated  immediately  above 
the  corpora  quadrigemina  has  led  to  softening,  especially 
of  the  right  half  of  the  tegmentum  (7')  and  of  the  region 
about  the  corpora  quadrigemina.  The  patient,  a  man  of 
fift3^-three,  presented  the  following  symptoms:  Headache, 
attacks  of  vertigo,  paresis  of  the  left  arm  and  leg,  marked 
hemianesthesia  of  the  same  side,  paralysis  of  the  muscles 
of  the  right  eye  (ptosis,  paralysis  of  the  sphincter  pupillse, 
superior  rectus,  etc.). 

Abbreviations. — AS,  Aqueduct  of  Sylvius;  N  III,  oculo- 
motor nerve;  ab,  basal  artery. 

Fig.  2. — Caries  of  a  Vertebra.  The  specimen  was  taken 
from  a  woman  forty-five  years  of  age  who  was  taken  ill 
with  pains  in  the  back  and  ribs,  accompanied  wdth  in- 
creasing weakness  in  the  legs.  At  the  end  of  three  months 
she  was  barely  able  to  stand,  and  slight  disturbances  of  the 
vesical  function  and  of  sensibility  made  their  appearance. 
Tendon  reflexes  increased;  irregular  fever;  nothing  abnor- 
mal in  the  vertebral  column.  Eventually  paralysis  of  the 
legs  resulted,  and  contractures  appeared.  The  appearance  of 
a  cold  abscess  in  the  thorax  gave  the  diagnosis :  Compres- 
sion of  the  spinal  cord  by  caries  of  the  vertebral  column. 

Autopsy. — Carious  focus  in  the  eighth  thoracic  vertebra 
(C);  exuberant  granulations  and  masses  of  caseous  mate- 
rial completely  filled  the  vertebral  canal  and  compressed 
the  spinal  cord  and  emerging  roots  (r).  r.  Body  of  ver- 
tebra; pr.  sp,  spinous  process;  d,  dura  mater. 

Fig.  3. — A  tumor  (T)  which  developed  on  the  inner  sur- 
face of  the  dura  (d)  in  the  vertebral  canal  in  a  woman 
thirty-eight  years  of  age,  and  gave  rise  to  severe  pains, 
referred  especially  to  both  legs,  in  the  course  of  three 
months  led  to  complete  spastic  paralysis  of  the  legs,  com- 
plete anesthesia  in  those  members  (the  only  trace  of  sensa- 
tion was  that  contact  wath  cold  water  gave  the  sensation  of 
heat),  incontinence  of  urine,  etc.  Death  from  cystitis  and 
pyelitis. 

Diagnosis. — Compression  of  the  spinal  cord  (carci- 
noma?). The  tumor  proved  to  be  a  sarcoma  which  filled 
the  vertebral  canal  at  a  level  corresponding  to  the  interval 
between  the  second  and  sixth  thoracic  vertebrae. 

Abbreviations. — v,  Body  of  vertebra;  r,  posterior  roots; 
d,  dura  mater;  prsp,  spinous  process. 


PLATE  60. 

Fig.  1. — Brain  Abscess.  A  woman  of  fifty-six  who  for 
years  had  complained  of  persistent,  dull  headache  and 
attacks  of  vomiting,  developed  gradually  increasing  fever 
and  fell  into  a  typhoid  state,  with  marked  rigidity  of  the 
neck,  trismus,  opisthotonos,  vomiting,  and  violent  head- 
ache. The  patient's  conversation  was  confused;  she  could 
not  find  the  right  name  for  ordinary  objects  with  the  use  of 
which  she  was  perfectly  well  acquainted,  such  as  fork, 
candle,  etc.  (optic  aphasia). 

At  the  autopsy  an  abscess  was  found  in  the  left  occip- 
ital lobe,  the  white  matter  of  which  had  been  largely 
destroyed. 

The  specimen  shows  a  horizontal  section  through  the 
occipital  lobe.  Pre,  Precuneus;  c,  cuneus;  o  s,  superior 
occipital  convolution;  Pe,  inferior  parietal  convolution 
(pli  courbe). 

Fig.  2. — Tubercle  in  the  Pons.  Male,  aged  fifty.  Com- 
plained of  headache  and  vertigo  for  the  past  year.  During 
the  last  six  weeks  there  occurred  attacks  of  vertigo,  stag- 
gering gait  (cerebellar  ataxia),  vomiting,  pain,  rigidity  in 
the  neck.  Right  side,  paresis  of  the  muscles  of  the  face,  arm, 
and  leg;  left  side,  paralysis  of  the  trigeminus  and  facial 
(facial  anesthesia)  (hemiplegia  alternans).  Inability  to 
rotate  the  eyes  first  to  the  left,  and  later  also  to  the  right; 
diplopia.  Later,  paralysis  of  the  muscles  of  the  pharynx 
and  of  the  vocal  cords;  cachexia;  death  after  eight  weeks. 
No  other  signs  of  tuberculosis. 

Diagnosis. — Tumor  of  the  base  of  the  brain  in  the  region 
of  the  pons. 

Specimen. — Large  tuberculous  tumor  (T)  in  the  left 
half  of  the  pons;  above  it,  in  the  tegmental  region  (tg),  a 
purulent  focus;  the  fourth  ventricle  has  been  pushed  up- 
ward; the  median  raphe  (R)  has  been  displaced  to  the 
right.  Destruction  of  the  middle  peduncle  of  the  cere- 
bellum (Prp),  of  the  pyramidal  tract  (Py),  of  the  trigem- 
inus, and  of  the  region  of  its  nucleus  and  of  the  nucleus 
of  the  .facial  nerve.    (Consult  Plates  38  and  39  for  letters. ) 


Tab,  60. 


Pre. 


Figl. 


Eig.2. 


Lith.  Anst.F.  Reichtiold,  Miincheri. 


'I'ah.  HI. 


bufX. 


PLATE  61. 

Fig.  1. — Chronic  Hydrocephalus.  Section  through  the 
middle  of  the  brain  of  an  idiot  eighteen  years  old,  the 
subject  of  congenital  hydrocephalus.  The  lateral  ven- 
tricle (ventr.  lat),  the  descending  horn  {v.inf),  and  the 
third  ventricle  (v.m)  are  very  much  dilated.  Flattening 
of  the  cortical  convolutions;  marked  reduction  in  the  thick- 
ness of  the  corpus  callosuni  (cc),  of  the  radiation  of  the 
corpus  callosum,  and  of  the  association  fibers,  the  projec- 
tion fibers  being  comparativelv  best  preserved.  (Consult 
Plate  38,  Fig.  2,  for  letters.) 

Fig.  2. — Acute  Hemorrhagic  Encephalitis.  Section  through 
the  left  occipital  lobe  of  a  woman  sixty-six  years  of 
age.  The  patient  was  seized  with  fever  and  vomiting 
and  presented  meningitic  symptoms.  The  most  marked 
symptom  was  a  constant  right-sided  hemianopsia;  the 
patient  was  unable  to  see  any  object  on  her  right  side 
until  it  was  carried  beyond  the  middle  of  the  visual  field  to 
the  left  side.  Death  occurred  at  the  end  of  thirteen  days 
after  increasing  coma,  rigidity  of  the  neck,  and  delirium. 

Autopsy. — Softening  of  the  basal  portion  of  the  tem- 
poral lobe,  of  the  mesial  and  basal  corti('al  convolutions 
of  the  left  occipital  lobe,  with  numerous  pinhead-sized 
hemorrhages. 

The  specimen  shows  hemorrhagic  encephalitis  with  soft- 
ening of  the  cuneus  (cun),  of  the  lingula  {ling)  and  its 
white  matter,  and  of  the  optic  radiation,  g.ang,  Gyrus 
angularis;  Praec,  precuneus;  fc,  calcarine  fossa. 


PLATE  62. 

Fig.  1. — Subcortical  Cerebral  Focus  after  Hemorrhage. 
Secondary  Degeneration.  A  woman  forty -two  years  of  age 
had  an  apoplectic  attack  which  left  the  following  residua: 
Total  motor  aphasia,  total  right-sided  hemiplegia  of  the 
face,  arm,  and  leg,  slight  hemianesthesia. 

Autopsy. — Extensive  destruction  of  the  white  matter 
under  the  central  convolutions  by  an  old  hemorrhage. 

Specimen. — The  focus  (/)  includes  the  white  matter  of 
the  posterior  central  convolution  (cp),  the  lateral  portion 
of  the  centrum  semiovale,  and  the  upper  portion  of  the 
internal  capsule  (ci).  From  the  focus  the  secondary  de- 
generation has  spread  to  the  corpus  callosum  (cc),  to  the 
internal  capsule  (x),  and  to  the  lateral  nucleus  of  the  optic 
thalamus  (Tho).  At  the  surface  of  the  pes  (ped)  the  seat 
of  the  degenerated  pyramidal  tract  is  represented  by  two 
bright  spots  separated  by  the  transverse  fibers  of  the  ansa 
lenticularis.      (See  Plate  31  for  further  explanations.) 

Fig.  2.  —  Embolic  Softening.  Secondary  Degeneration. 
Section  through  the  occipitoparietal  lobe  of  a  man  forty- 
five  years  of  age.  The  patient  suffered  from  mitral  stenosis 
and  had  had  several  apoplectic  attacks  due  to  embolism. 
One  of  these  attacks  left  him  with  a  pronounced  right- 
sided  homonymous  hemianopsia. 

Autopsy. — Numerous  cysts  due  to  emboli  and  scars  were 
found  all  over  the  brain. 

Sj)eciynen. — Softening  of  the  cuneus  {cun)  and  of  the 
lingula  (ling)  and  its  white  matter.  Secondary  degene- 
ration of  the  inferior  longitudinal  bundle  and  Gratiolet's 
optic  radiation  (o).     (Compare  Plate  33,  Fig.  1.) 


Tab.  (i'J 


Fiff.l. 


i    >■ 


Fiif.:^. 


Tab.ff.-i. 


0 


<^5?  . 


ligJ 


,,..'.' JlV-^-^-r., 


%^^ 


Fig.3. 


Litfh.  Aast.  F.  ReichJwLd,  Munxlwi- 


PLATE  63. 

Figs,  a  to  f.  — Products  of  Degeneration  of  Nerve-cells  and 
Fibers,  (a)  Degenerating  nerve-fibers  (longitudinal  sec- 
tion from  a  case  of  alcoholic  neuritis) ;  {b)  swollen  and 
degenerating  fibers,  transverse  section  from  a  case  of  acute 
m^-elitis;  (c)  fibers  and  cells  from  the  cerebral  cortex, 
filled  with  fat  droplets,  treated  with  osmic  acid  (from  a 
case  of  thrombotic  softening);  {d)  fatty  granule  cells,  un- 
stained; {e)  atrophic  ganglion  cells  from  the  nucleus  of 
the  hypoglossus  (from  a  case  of  bulbar  palsy);  (/)  cells 
containing  blood  pigment,  fragments  of  hemoglobin  (from 
a  case  of  cerebral  hemorrhage) ;  {g)  corpora  aniylacea 
from  the  posterior  column  (from  a  case  of  tabes  dorsalis). 

Fig.  1. — Specimen  of  Acute  Myelitis.  (One  hundred  and 
fifty  diameters).  Taken  from  the  case  shown  in  Plate  75, 
Figure  1.  The  microscope  shows  in  the  lateral  cord  mye- 
litic foci  separated  by  areas  of  normal  tissue.  Instead  of 
the  closely  packed  nerve-fibers  stained  blue-black  we  see 
vacuoles;   the  fibers  present  all  the  stages  of  degeneration. 

Fig.  2. — Specimen  of  Acute  Neuritis.  Portion  of  a  nerve 
bundle  from  the  sciatic  nerve  from  a  case  of  alcoholic 
neuritis.  Great  destruction  of  nerve-fibers  ;  only  a  few 
bluish-black  fibers  remained.  The  sites  of  the  medullary 
sheath  can  be  recognized  in  the  connective-tissue  stroma 
and  in  the  thickened  sheath  of  Schwann. 

Fig.  3. — Specimen  of  Chronic  Sclerosis.  Section  through 
the  lateral  column  from  a  case  of  amyotrophic  lateral  scle- 
rosis. In  consequence  of  the  gradual  disappearance  of  the 
pyramidal  tracts  the  neurogliar  tissue  is  greatly  increased; 
here  and  there  a  few  isolated  nerve-fibers  are  seen  in  trans- 
verse section. 

Fig.  4. — Specimen  of  Chronic  Myelitis.  Section  through 
the  lateral  column  from  an  old  case  of  myelitis.  Com- 
plete loss  of  the  nerve-fibers,  dense  network  of  neurogliar 
tissue,  indurated  sheaths  of  blood-vessels  surrounded  by 
the  remains  of  old  hemorrhages  (fragments  of  blood  pig- 
ment), characterize  this  myelitic  *'scar." 


PLATE  fi4. 
Diseases  of  the  Muscle=fibers. 

Fig.  1. — Transverse  section  of  a  normal  muscle  com- 
posed of  bundles  of  equal  size,  presenting  a  polygonal 
shape  in  transverse  section  and  containing  a  few  cells. 

Figs.  2  and  3. — Transverse  and  Longitudinal  Sections  of 
Muscle  in  Spinal  Muscular  Atrophy  (Biceps).  There  is  a 
marked  A^ariation  in  the  thickness  of  the  individual  fibers; 
some  of  them  have  disappeared  entireh^  others  are  much 
reduced  in  size  (p).  The  muscle  nuclei  are  much  increased 
and  form  the  so-called  ' '  lines  or  verses  of  nuclei "  (  "  Kern- 
zeilen").  The  transverse  striation  of  the  protoplasm  is 
lost  in  the  degenerated  fibrils;  the  protoplasm  itself  has 
undergone  degeneration,  n,  Normal  fi})rils  ;  h,  h^'per- 
trophic  fibrils. 

Fig.  4. — Juvenile  Muscular  Atrophy  (Dystrophia  Muscu- 
laris  Progressiva)  (Quadriceps  Extensor).  Whole  bundles 
of  muscle-fibers  are  destroyed,  the  nuclei  are  increased  in 
number,  and  many  fibers  are  hypertrophic.  Transverse 
striation  is  preserved  for  some  time  in  spite  of  the  atrophy 
of  the  fibers.  The  intervals  between  the  remaining  mus- 
cular fibers  are  frequently  filled  with  fat  (pseudohyper- 
trophy). At h so-called  "hypertrophic "  muscle-fibers;  ?i, 
normal  fibers. 

Fig.  5. — Neurotic  Muscular  Atrophy  (opponens  pollicis). 
The  section  shows  marked  diminution  in  the  size  of  the 
fibrils  and  increase  in  the  number  of  nuclei.  The  trans- 
verse striation  persists  for  some  time. 

Fig.  6.  —  Unstained  Muscle-fibers,  (a)  Degenerative  mus- 
cular atrophy  (quadriceps  extensor  from  a  case  of  lumbar 
myelitis).  The  muscle  is  granular  and  cloudy,  the  fibrils 
are  broken  up,  the  transverse  striation  has  disappeared, 
and  the  fibers  are  reduced  in  thickness,  but  not  uniformly. 
Eventually  the  disintegrated  protoplasm  is  absorbed  and 
nothing  but  the  empty  tube  of  sarcolemma  remains,  (h) 
Neurotic  muscular  atrophy,  slight  diminution  in  the  thick- 
ness of  the  fibers  with  "lines  of  nuclei "  and  well-marked 
transverse  striation  (see  above). 


Tab.  64. 


Fig.  4^. 


I.Lth.  Aiist  t:  ReichhxM.  Mimchen. 


Tab.  65. 


Fig.  1. 


crrh 


Fig.  2. 


PLATE  65. 

Fig.  1. — Left  hemisphere  from  a  man  fifty-six  years  of  age,  who, 
after  several  attacks  of  apoplexy,  was  left  with  a  permanent  complete 
spastic  paralysis  of  the  right  facial  and  hyx)Oglossus  and  of  the  right 
arm,  and  with  weakness  of  the  right  leg  (right-sided  hemiplegia).  He 
had  also  lost  the  power  of  volnntary  speech  (motor  aphasia) ;  inability 
to  understand  spoken  and  written  language  (word-deafness,  loss  of 
visual  memory  pictures) .  The  dementia  gradually  increased  and  death 
occurred  after  three  years. 

The  photograph  shows  the  outer  surface  of  the  left  hemisphere.  A 
large  portion  of  the  cortical  convolutions  is  destroyed  (porencephalus). 
The  following  portions  of  the  cortex  have  been  converted  into  con- 
nective tissue  :  The  posterior  portion  of  the  middle  and  inferior  frontal 
convolution  {g.  fr.  m  and  «'),  the  superior  and  middle  temporal  convo- 
lutions {g.  f.  s  and  m),  the  inferior  parietal  lobule  [l.  p.  i),  the  greater 
portion  of  the  anterior  and  posterior  central  convolutions,  esp-jcially 
the  lower  half  (</.  c.  a  and^),  and  the  central  portion  of  the  occipital 
lobe  (o).  The  destructive  process  extends  underneath  the  cortex  and 
involves  large  portions  of  the  insula  ( / )  and  of  the  white  matter  of  the 
hemispheres.  /,  S,  Fissure  of  Sylvius;  S.  R,  fissure  of  Rolando;  Ch, 
cerebellum. 

Fig.  2.  —  View  of  the  Intei-ior  of  the  Third  Ventricle  after  Removal  of 
the  Corpus  Callosum  and  Fornix.  The  left  optic  thalamus  and  surround- 
ing structures  (corpora  quadrigemina,  internal  cai)sule)  are  completely 
destroyed. 

A  man  fifty  years  of  age  had  a  stroke  of  apoplexy;  when  he  recov- 
ered, after  three  days  of  coma,  he  was  paralyzed  on  the  right  side  (face, 
arm,  and  leg) ;  at  the  same  time  there  was  oculomotor  paralysis  of  the 
left  eye  (hemiplegia  alternans).  There  was  no  disturbance  of  speech, 
but  there  was  a  right-sided  hemianesthesia. 

The  focus  was  found  to  be  very  extensive  and  due  to  hemorrhage. 
Under  the  optic  thalamus  of  the  left  side  the  subthalamic  region,  and 
further  out  the  posterior  limb  of  the  internal  capsule,  were  destroyed. 
Also  the  left  anterior  corpus  quadrigeminum  (c.  q.  a)  and  the  tegmental 
region,  including  the  left  oculomotor  nucleus.  Th,  Optic  thalamus; 
Pill,  pulvinar;  c.  m,  middle  commissure,  central  portion;  c.  a,  anterior 
horn  of  the  lateral  ventricle;  C.  st,  corpus  striatum;  c.  c,  corpus  cal- 
losum; cqp,  left  posterior  corpus  quadrigeminum. 


PLATE  66. 

Fig.  1. — Section  through  the  Anterior  Corpora  Quadrige- 
mina.  The  left  tegmental  region  (/)  is  completely  de- 
stroyed; the  left  corpus  quadrigeminum  (cqa)  is  atrophied. 
The  region  about  the  nucleus  of  the  left  oculomotor  (iV. 
///),  underneath  the  aqueduct  of  Sylvius  (A.  S),  is  like- 
wise destroyed.  Complete  absence  of  the  constituents  of 
the  tegmentum,  red  nucleus  (n.  r),  superior  and  inferior 
fillet  (L),  substantia  reticularis,  etc.;  the  entire  left  half 
of  the  crusta  (ped  x)  is  atrophied.  Clinical  symptoms  as 
in  Plate  65,  Figure  2:  Hemiplegia  alternans. 

Fig.  2. — Section  through  the  Medulla  Oblongata  of  a  Young 
Girl,  the  Subject  of  Hereditary  Tuberculosis.  The  patient  was 
taken  ill  quite  suddenly  with  headache,  vomiting,  and  in- 
creasing weakness  of  the  right  leg,  and  later  of  the  right 
arm.  This  was  soon  followed  by  paralysis  of  the  left  facial 
and  hypoglossus  (hemiplegia  alternans),  and  paralysis  of 
the  muscles  of  the  pharynx.  Sudden  death.  At  the  au- 
topsy a  tumor  was  found  in  the  pons  which  had  spread 
far  into  the  medulla  {Tab)  and  destroyed  the  pyramids 
{Py\  and  the  facial  and  hypoglossus  (XII)  nerves  at  their 
points  of  exit.  The  tumor  proved  to  be  a  solitar}^  tubercle 
containing  large  numbers  of  giant  cells. 

Fig.  3.  — So  far  we  have  considered  focal  diseases  of  the 
brain.  The  specimen  before  us  shows  a  system  disease 
— namely,  chronic  progressive  ophthalmoplegia.  The  cells  of 
the  oculomotor  nucleus  (N.  Ill)  are  the  seat  of  a  primary 
degeneration,  and  the  fibers  of  the  oculomotor  nerve 
(N.  Ill),  which  normally  form  a  massive  bundle  at  their 
point  of  exit  on  the  surface  of  the  brain,  have  also  dis- 
appeared. (Compare  the  corresponding  normal  section, 
Plate  40,  Fig.  2. ) 

The  disease  occurred  in  a  woman  suffering  from  tabes 
dorsalis.  Paralysis  of  all  the  ocular  muscles  had  gradu- 
ally developed,  c.  p,  Posterior  commissure;  S.  n,  sub- 
stantia nigra;  n.  r,  red  nucleus;  Ped,  crusta;  I,  fillet. 


Tab.  66. 


Fig.  1. 


Fig. 


Fig.  3. 


Tab.  67. 


Fig.  1. 


Tho 


Fig.  3. 


PLATE  67. 
Secondary  Degenerations  of  the  Crusta. 

Figures  1  and  2  present  transverse  sections  through  the  anterior  cor- 
pora quadrigemina  and  the  parts  immediately  below  these  structures. 
There  is  complete  atrophy  of  the  fibers  in  the  right  half  of  the  crusta 
(x).  The  specimens  were  taken  from  a  case  with  extensive  primary 
destruction  of  the  cerebral  cortex.  As  the  fibers  in  the  crusta  have 
their  neuron  cells  in  the  cortex,  they  necessarily  undergo  a  secondary 
descending  degeneration  if  these  cells  are  destroyed. 

The  tract  of  the  fillet  (Z<)  on  the  right  side  is  narrower  than  on  the 
left,  but  the  degeneration  is  not  complete  (simple  nondegenerative 
atrophy).  The  neuron  cells  of  the  fibers  in  the  fillet  are  not  situated 
in  the  cortex,  but,  in  part  at  least,  in  the  funiculus  gracilis  and 
cuneatus,  while  others  are  probabl}^  to  be  sought  in  the  subthalamic 
region  and  in  the  optic  thalamus.  (The  clinical  symptom  in  this  case 
was  a  total  left-sided  hemiplegia.)  The  red  nucleus  {nr)  is  also 
atrophic.     The  anterior  and  posterior  brachia  have  disappeared. 

AhhreviaHons.—tr.  o,  Optic  tract;  S.  n,  substantia  nigra;  L,  fillet; 
c.  q.  a,  anterior  corpus  quadrigeminum;  Ped,  crusta. 

Fig.  3. — Section  through  the  Anterior  Corpora  Quadrigemina  in  Total 
Secondary  Atrophy  of  the  3fesial  Fibers  of  the  Crusta  {Frontal  Pontine 
Tract)  [x).  This  partial  degeneration  of  the  crusta  ( Ped)  was  secondarj^ 
to  an  embolic  softening  focus  which  had  destroyed  the  anterior  limb 
of  the  capsule  and  the  lenticular  nucleus.  There  were  no  clinical 
symptoms. 

Abbreviations. — A.  S,  Aqueduct  of  Sylvius;  c.g.m,  mesial  geniculate 
body;  eg,  lateral  geniculate  body;  c,  pineal  gland;  Z,  fillet;  e.  q.  a, 
anterior  corpora  quadrigemina;  nr,  red  nvicleus;  N.  Ill,  oculomotor. 

These  and  the  following  examples  of  secondary  degenerations  in  the 
brain  and  spinal  cord  are  particularly  important  from  a  neurological 
point  of  view,  because  they  enable  us  to  follow  the  course  of  the 
various  pathways  almost  as  accurately  as  could  be  done  in  actual  ex- 
perimental work.  They  represent  in  man  the  experimental  work  done 
on  animals.  It  is  for  this  reason  that  we  have  described  them  here  at 
some  length.  They  are  well  adapted  to  illustrate  once  more  the  text 
in  Part  III. 


PLATE  68. 
Secondary  Degenerations  of  the  Crusta. 

Fig.  1.— Section  througli  the  Third  Ventricle  {Middle  Commissure). 
Beneath  the  optic  thalamus  (Th),  which  has  been  cut  away,  are  the 
constituents  of  the  subthalamic  region,  the  subthalamic  body  (c.  Z), 
white  matter  of  the  nucleus  {L)  and,  underneath,  the  internal  capsule 
(c{,  posterior  limb),  above  the  point  where  it  becomes  the  pes.  On  the 
right  side  the  middle  portion  {x)  of  the  internal  capsule  is  degenerated 
in  consequence  of  a  lesion  (hemorrhage)  which  has  destroyed  the  cen- 
tral convolutions. 

The  degenerated  areas  correspond  to  a  portion  of  the  pyramidal 
tract,  tro,  Optic  tract;  cm,  middle  commissure;  /,  fornix;  v  III,  third 
ventricle. 

Fig.  2. — Section  through  the  Anterior  Corpora  Quadrigemina,  from  the 
same  Case.  The  figure  shows  the  position  of  the  degenerated  pyramidal 
tract  (Py)  in  the  middle  of  the  crusta  {Fed).  A  large  i)ortion  of  the 
tract,  however,  which  in  this  case  is  not  totally  degenerated,  occupies 
a  larger  area  situated  laterally  from  the  diseased  portion.   (See  Fig.  3.) 

Clinically  there  was  a  left-sided  hemiparesis  of  the  face,  arm,  and 
leg.  A.S,  Aqueduct;  L,  fillet;  cgm,  lateral  geniculate  body;  cqa,  an- 
terior corpus  quadrigeminum;  III,  oculomotor;  nr,  red  nucleus;  Sn, 
substantia  nigra. 

Fig.  3. — In  this  case,  which  belongs  to  Plate  62,  Figure  1,  there  is 
a  pure  degeneration  of  the  pyramidal  tract  ( p^.  To  its  lateral  side  we 
see  the  oval  bundle  of  Tiirck  (o)  in  the  crusta;  m,  the  mesial  pontine 
tract;  T,  optic  thalamus;  B,  red  nucleus;  L,  superior  fillet;  g,  lateral 
geniculate  body. 

Owing  to  the  secondary  shrinking  which  always  takes  place,  these 
cases  of  degeneration  do  not  represent  accurately  the  entire  extent  of 
the  degenerated  bundle. 


Tab.  68. 


Fig.  1, 


Tab.  69. 


Fig.  2. 


PLATE  69. 
Secondary  Degenerations  of  the  Pons. 

Fig.  1. — Section  through  the  Anterior  Half  of  the  Pons. 
The  section  belongs  to  the  case  shown  on  Plate  67,  Figures 
1  and  2.  On  the  left  side  the  peduncular  fibers  collected 
in  numerous  bundles  are  seen  traversing  the  transverse 
pontine  fibers  (P) .  On  the  right-hand  side  (x)  these  fibers, 
as  well  as  the  pontine  ganglia,  are  completely  wanting;  hence 
the  enormous  diminution  in  the  width  of  the  right  side  of 
the  pons.  We  learn  from  this  section  that  the  secondary 
degeneration  does  not  confine  itself  to  the  fibers  connecting 
two  ganglion  systems  directly  continuous  with  one  an- 
other by  their  neurons,  but  extends  also  to  their  cells. 
The  fillet  (Ls,  i)  is  atrophic. 

Abbreviations. — B,  Brachium;  v.  IV,  aqueduct  of  Sylvius; 
/,  posterior  longitudinal  bundle. 

Fig.  2. — Section  through  the  Middle  of  the  Pons,  with  Exten- 
sive Secondary  Degenerations  in  the  Tegmental  Region.  The 
specimen  belongs  to  the  case  shown  on  Plate  65,  Figure  2. 
(The  photograph  is  inverted  so  that  the  left,  diseased  half 
is  shown  on  the  right  side. )  The  degeneration  includes 
the  two  brachia  (B)  (in  part  on  the  right  side  at  2);  the 
neuron  cells  are  in  the  red  nucleus,  which  has  been  de- 
stroyed. The  central  tract  of  the  fillet  (c.  t)  in  the  right 
half  of  the  tegmentum,  the  entire  superior  fillet  (7/)  (neu- 
ron cells  in  the  destroyed  subthalamic  region  and  in  the 
optic  thalamus?), the  right  pyramidal  tract  (Pi/)  and  other 
tracts,  the  substantia  reticularis,  and  other  structures. 
Vm,  Motor,  Vs,  sensory,  nucleus  of  the  trigeminus;  be- 
tween the  two  the  descending  root  (  Vc) ;  /,  posterior  lon- 
gitudinal bundle;  v,  superior  vermiform  process;  P,  pon- 
tine ganglia;    Vn,  nasal  root  of  the  trigeminus. 


PLATE  70. 
Secondary  Degenerations  in  the  Medulla  Oblongata. 

P'iG.  1. — Section  through  the  Medulla  Oblongata  below  the  Pons.  The 
entire  left  pyramidal  tract  (x)  has  undergone  secondary  degeneration, 
owing  to  primary  destruction  of  the  posterior  limb  of  the  internal  cap- 
sule by  hemorrhage  (right-sided  hemiplegia);  the  fillet  (/>)  is  reduced 
in  size. 

Note  in  this  section  the  course  of  the  striae  acusticai  {stra)  on  the  left 
side,  from  the  central  nucleus  of  the  auditory  nerve  over  the  floor  of  the 
fourth  ventricle  to  the  raphe,  where  they  undergo  decussation  and  pass 
to  the  fillet.  Cb,  restiform  body;  NVIJ,  nucleus  of  facial  nerve;  Nx, 
nucleus  of  vagus;  Py,  pyramidal  tract. 

Fig.  2. — Medulla  Oblongata  in  Infantile  Cerebral  Parali/siH.  The 
specimen  was  taken  from  a  man  thirty  years  of  age,  who  from  his 
earliest  infancy  (congenital?  acquired?)  presented  the  marks  of  ar- 
rested development  in  the  entire  right  half  of  the  body.  The  right  arm 
was  paretic,  and  there  was  a  moderate  contracture  of  the  flexor  muscles. 
There  was  also  weakness  of  the  right  leg.  Epileptiform  attacks. 
Athetosis. 

Le-^hofa™ i^'^"^- 

Arm.  Forearm. 

rircumference  <  ^^^^*'  ^^  ^"'-    ^^^^*'  ^^^"'• 

Circumterence |  ^ef t,    24  "      Left,     24  " 

Circumference  of  thigh    .   JLeft^^'sg^^* 

p  ,.  _  (Right,  29  cm. 

^^^      \Left,     32  " 

Autopsy. — The  left  central  convolutions  were  rudimentary  (agene- 
sis?). The  entire  left  pyramid  (x)  was  atrophied,  as  was  the  left  fillet 
iy)j  although  there  was  no  true  degeneration,  evidently  because  the 
disease  made  its  appearance  at  a  time  when  medullarization  had  not 
yet  begun.  The  raphe  {k)  is  displaced  to  the  left;  the  right  pyramid 
is  almost  hypertrophic  (topical  compensation),  cr,  Restiform  body; 
ol,  inferior  olive;  XII,  nucleus  of  hypoglossus. 

Fig.  '^.—3Iedulla  Oblongata  in  Atrophy  of  the  Fillet — The  right  fillet 
{L.  x)  and  the  internal  arcuate  fibers  [fai,  y)  of  the  substantia  reticu- 
laris (8.  r)  of  the  leftside  (!)  show  a  descending  degeneration.  These 
arcuate  fibers  correspond  to  the  direct  communication  with  the  fillet 
of  the  opposite  side,  which,  with  the  funiculus  gracilis  and  funiculus 
cuneatus  (w.  C?),  appear  in  the  restiform  body  (O).  The  pyramid 
{Py.  x)  and  the  olives  (o?)  of  the  same  side  are  also  degenerated. 

The  chief  clinical  symptom  was  hemianesthesia  of  the  left  half  of 
the  body.     (See  Plate  65,  Fig.  2,  to  which  this  specimen  belongs.) 


Tab.  70. 


Fig.l. 


Fig:  3. 


Tab.  71. 


Fig.l. 


■^■aKiJtr'- "' 


!      Fig.  2. 


Fig. 


PLATE  71. 

Descending  Degeneration  of  the  Pyramidal  Tract  in  the  Spinal 
Cord  after  a  Focal  Lesion  of  the  Cerebrum. 

The  specimens  belong  to  the  case  illustrated  on  Plate  70, 
Figure  1,  where  the  left  pyramid  shows  secondary  degener- 
ation throughout.  This  degeneration  can  be  traced  in  the 
spinal  cord  through  the  entire  course  of  this  tract — that  is 
to  say,  below  the  decussation  of  the  pyramids  in  the  lat- 
eral column  of  the  opposite  (right)  side  (crossed  fibers), 
and  in  the  anterior  column  of  the  same  side  (uncrossed 
fibers). 

In  the  cervical  and  thoracic  portions  of  the  cord  the  lat- 
eral pyramidal  tract  {Py)  is  bounded  on  the  outer  side  by 
the  direct  cerebellar  tract,  which  is  still  preserved.  In  the 
lumbar  portion  of  the  cord  the  cross-secti6n  is  wedge- 
shaped  and  extends  to  the  periphery.  The  degeneration 
of  the  anterior  pyramidal  tract  {x)  can  be  traced  into  the 
lower  thoracic  portion  of  the  cord.  In  the  right  anterior 
horn  the  destruction  can  be  seen  with  the  microscope.  The 
degeneration,  therefore,  involves  the  central  motor  neuron 
complex,  the  entire  pyramidal  tract,  so  that  the  entire 
right  side  of  the  spinal  cord  is  considerably  diminished  in 
size. 

Fig.  1. — Cervical  Portion  (Sixth  Cervical  Nerve). 

Fig.  2.  —  Thoracic  Portion  (Third  Dorsal  Nerve). 

Fig.  3. — Lumbar  Portion  (Second  Lumbar  Nerve). 

Fig.  4. — Sacral  Portion. 


PLATE  72. 

Descending  Degeneration  in  the  Spinal  Cord  in  Diseases  of 
the  Spinal  Cord. 

Fig.  1. — Lower  Cervical  Portion  of  the  Cord. 

Fig.  2. — Lower  Thoracic  Portion.  (The  figure  is  inverted  so  that 
the  right  half  appears  on  the  left  side. ) 

Fig.  3.  —  Upper  Lumbar  Portion.  The  specimens  were  taken  from 
a  man  forty  years  of  age  who  fell  and  sustained  a  fracture  of  a  cervical 
vertebra,  followed  by  contusion  of  the  lower  cervical  portion  of  the 
cord.  The  following  symptoms  were  present:  Complete  spastic  para- 
plegia of  the  legs,  muscular  atrophy  and  paralysis  of  the  small  muscles 
of  the  hand,  anesthesia,  incontinence  of  urine. 

Autopsy. — Below  the  point  of  compression  in  the  cervical  portion 
of  the  cord  there  was  found  a  descending  degeneration  of  both  lateral 
pyramidal  tracts  {Py)  and  anterior  pyramidal  tracts  [Pya),  and  of  a 
comma-shaped  area  (r,  Schultz'  area,  containing  descending  fibers 
arising  from  the  gray  matter)  in  the  columns  of  Burdach  and  a  central 
area  ("clearing")  in  the  columns  of  Goll.  Note  that  the  anterior 
pyramidal  tract  on  the  right  side  is  considerably  smaller  than  on  the 
left  (individual  variation).  In  the  thoracic  and  lumbar  portions  of 
the  cord  the  pyramidal  tracts  on  both  sides  are  degenerated.  The 
degeneration  of  the  posterior  columns  has  disappeared  (short  path- 
ways). 

Fig.  4. — Lumbar  Portion  of  the  Cord  in  Compression  of  the  Thoracic 
Portion.  The  specimen  was  taken  from  the  case  shown  on  Plate  59, 
Figure  3.  Sarcoma  of  the  dura  mater.  Below  the  seat  of  compression 
there  was  descending  degeneration  of  the  pyramidal  tracts  {Py)  on 
both  sides,  and  some  degeneration  in  the  marginal  zone  of  the  antero- 
lateral column  (fal)  (descending  branches  of  the  central  sensory 
neurons  arising  in  the  gray  matter)  (middle  zone). 

Note  the  great  number  of  fibers  entering  the  anterior  horns  from 
the  posterior  horn  and  posterior  roots. 


Tab.  72. 


I  Fig.  1. 


Tab.  73. 


Fig.  2. 


..^-s-s-:;^  ^:P: 


Fig.3^ 


PLATE  73. 
Ascending  Degeneration  of  the  Spinal  Cord. 

A  soldier  twenty-two  years  of  age  fell  and  crushed  the 
lower  thoracic  portion  of  the  vertebral  column  and  suffered 
a  contusion  of  the  lumbar  cord.  Complete  flaccid  paral- 
ysis of  the  legs  ensued,  and  was  followed  by  a  rapidly  de- 
veloping degenerative  muscular  atrophy.  Disturbance  of 
sensation,  bladder,  and  rectum,  and  loss  of  patellar  reflex. 
The  patient  died  two  months  later  of  cystitis. 

Fig.  1.  —  Upper  Contused  Portion  of  the  Lumbar  Cord. 

Fig.  2. — Middle  Thoracic  Portion.  There  is  a  secondary 
ascending  degeneration  of  the  columns  of  Goll  (JG)  (neu- 
ron cells  in  the  spinal  ganglia). 

Fig.  3. — Lower  Cervical  Cord.  The  degenerated  columns 
of  Goll  (fG)  present  a  distinct,  wedge-shaped  outline. 
They  occupy  a  mucli  smaller  area  than  in  deeper  sections. 

In  addition  we  note  an  ascending  degeneration  of  the 
left  direct  cerebellar  tract  (Cb)  and  of  Gowers'  tract  (6r) 
on-  the  left  side.  It  is  readily  seen  in  Figure  1  that  the 
gra}^  matter  and  the  columns  of  Clarke,  where  the  neuron 
cells  of  these  tracts  are  situated,  have  suffered  a  much 
greater  destruction  on  the  left  than  on  the  right  side. 

The  columns  of  Goll,  therefore,  contain  the  long  sensory 
pathways  from  the  lower  extremities,  and  are  joined  higher 
up  by  the  long  sensory  pathways  from  the  trunk  and 
upper  extremities  (column  of  Burdach). 

Abbreviations. — Ca,  Anterior  horn;  fa,  anterior  column; 
Jl,  lateral  column;  fp,  posterior  column;  Sa,  anterior 
sulcus. 


PLATE  74. 

Ascending  Degeneration  in  the  Cervical  Portion  of  the  Cord 
and  Medulla  Oblongata. 

Fig.  1. — Ascending  Secondary  Degeneration  in  the  Upper 
Cervical  Portion  in  Primary  Acute  Myelitis  situated  about  the 
Middle  of  the  Thoracic  Cord.  As  a  result  of  the  interrup- 
tion of  the  fibers  which  takes  place  in  the  thoracic  cord 
the  following  regions,  containing  long  pathways,  are  de- 
generated: Column  of  Goll  (f.G),  direct  cerebellar  tract 
(C6),  Gowers'"  tract  (G),  and  the  marginal  zone  of  the  an- 
terior column. 

Fig.  2. — Section  through  the  Decussation  of  the  Pyramids. 
Ascending  degeneration  in  chronic  (syphilitic?)  myelitis 
situated  in  the  thoracic  cord.  The  columns  of  Goll  (/.  G), 
the  direct  cerebellar  tract  (Cb),  and  Gowers'  tract  (G)  are 
degenerated. 

Fig.  3. — Section  through  the  Medulla  Oblongata  at  the  Level 
of  the  Inferior  Pole  of  the  Olive.  The  preparation  belongs  to 
the  case  illustrated  on  Plate  73,  and  represents  a  section 
immediately  below  that  shown  in  Figure  3. 

We  note  ascending  degeneration  of  the  columns  of  Goll 
(/.  G)  in  which  the  funiculi  graciles  (nuclei  of  Goll,  n  G) 
have  made  their  appearance.  The  degeneration  has  not 
extended  to  the  contiguous  fibers  of  the  fillet  (internal 
arcuate  fibers,  fai)^  which  therefore  represent  a  new,  inde- 
pendent neuron.  In  the  direct  cerebellar  tract  (Ch)  the 
degeneration  is  evidently  also  confined  to  the  left  side. 
Owing  to  the  obliquity  of  the  plane  of  section  the  right 
olive  only  is  included. 

Abbreviations. — L,  Fillet;  /.  a.  i,  internal  arcuate  fibers; 
ol.  m,  mesial  accessory  olive;  ol,  inferior  olive;  Sg,  sub- 
stantia gelatinosa;  fB,  fG,  columns  of  Burdach  and  Goll; 
n  B,  n  G,  funiculi  gracilis  and  cuneatus. 


Tab.  74. 


Fig.  1. 


V. 

SPECIAL  PATHOLOGY 


Spinal  Cord  and  of  the  Peripheral 

Nerves. 

(Part  V.  of  Text.) 


Tab.  75. 


Fig.  1. 


Fig.  2. 


Fig.  3. 


PLATE  75. 
Various  Forms  of  Myelitis. 

Fig.  1. — Columnar  Acute  (toxic)  MyelitiH.  (Cervical  portion  of  the 
cord. )  A  man  forty -two  years  of  age,  after  a  severe  attack  of  erysipelas, 
developed  a  rapidly  increasing  paresis  of  the  arms  and  legs,  accom- 
panied by  painful  sensations.  The  paralysis  was  never  complete. 
There  was  slight  disturbance  of  sensation  and  of  the  vesical  function ; 
pain-sense  remained  normal.  Toward  the  end  there  was  paralysis  of 
the  diaphragm.     The  disease  lasted  only  four  months. 

Diagnosis. — Multiple  neuritis  (?). 

Autopsy. — Extensive  myelitic  degeneration  of  the  posterior  columns 
(/•  ^T,  /.  B),  extending  from  the  cervical  to  the  thoracic  portion  of  the 
cord.  Myelitic  foci  in  the  lateral  columns  (Py),  especially  in  the  cer- 
vical region.  Slight  neuritic  changes.  This  case  proves,  among  other 
things,  that  the  posterior  columns  are  not  essential  to  cutaneous  sen- 
sation. 

Fig.  2.— Chronic  {syphilitic?)  Myelitis.  (Cervical  region.)  A  man 
forty-eight  years  of  age,  suspected  of  lues,  developed  a  slowly  pro- 
gressive weakness  of  the  legs,  without  pain,  which  after  a  year  and  a 
half  culminated  in  total  paraplegia  and  loss  of  all  sensation.  Knee- 
jerks  exaggerated.     Incontinence. 

The  specimen  shows  a  diffuse  myelitic  degeneration  involving  the 
entire  transverse  section  of  the  cord.  It  was  most  extensive  in  the 
region  includmg  the  seventh,  eighth,  and  ninth  thoracic  segments. 
Below  the  lesion  there  was  descending  degeneration  of  the  pyramidal 
tract.  (For  the  changes  above  the  lesion  consult  Fig.  2  on  Plate  74, 
which  belongs  to  this  case.) 

Fig.  3. — ^'  Compression  Myelitis.'' \  Carcinoma  in  the  third  thoracic 
vertebra  led  to  compression  of  the  cervical  cord,  folloAved  by  marked 
degeneration  in  every  part  of  the  cross-section. 

The  specimen  was  taken  from  a  woman  forty-two  years  of  age,  who 
was  suddenly  seized  with  violent  neuralgic  pains  in  the  back.  She 
rapidly  developed  a  progressive  paresis  of  the  legs  and  became  com- 
pletely bedridden.  There  were  disturbances  of  the  bladder  and  of 
sensation.  After  three  months  the  paraplegia  had  become  complete. 
Contractures  formed,  and  the  patient  suffered  continuously  from 
violent  pain  which  could  hardly  be  controlled  by  opium.  The 
disease  lasted  six  months. 

Abbreviations. — ca,  cp,  Anterior  horn,  posterior  horn;  cc^  central 
canal  ;j^,  fp,  lateral  column,  posterior  column. 


Fig.  4. 

PLATE  76. 
Syringomyelia. 

Fig,  1. — Hydromyelia,  Upper  Thoracic  Region.  (Specimen  of  Pro- 
fessor v.  Striimpell.)  A  man  thirty-five  years  of  age,  the  subject  of 
hereditary  disease,  developed  a  slowly  increasing  weakness  and  stiff- 
ness of  the  legs,  and  later  of  the  arms.  The  tendon  reflexes  were  ex- 
aggerated ;  muscular  spasms  appeared  and  gradually  grew  worse.  No 
atrophy.     Sensation  normal. 

Diagnosis. — Spastic  spinal  paralysis. 

Autopsy. — Hydromyelia  with  degeneration  of  the  pyramidal  tract. 
The  central  canal  throughout  the  spinal  cord  was  converted  into  a 
wide  cavity  filled  with  fluid  (hydromyelus).     Congenital  (?). 

Figs.  2  and  3. — Sections  through  the  Upper  and  3Iiddle  Thoracic 
Portions  of  the  Cord  from  another  case  of  Syringomyelia.  The  cavity 
extends  partly  into  the  anterior  and  into  the  iX)sterior  horns,  involving 
the  entire  extent  of  the  latter.  The  clinical  course  was  as  follows:  A 
man  forty  years  of  age  developed  slowly  progressive  weakness  and 
emaciation  of  the  right,  and  later  of  the  left,  hand  and  right  arm.  The 
muscles  of  the  ball  of  the  thumb,  the  hypothenar  muscles,  and  the 
interossei  were  the  first  to  undergo  degenerative  atrophy.  Pain-sense 
and  temperature-sense  were  completel}"  lost  in  the  arms.  The  tactile 
sense  was  normal.  Trophic  disturbances  made  their  appearance  in  the 
hands.  Inflammatory  necrotic  processes  in  the  phalanges,  nails,  and 
joints. 

Figure  2  shows  a  partial  descending  degeneration  of  the  column  of 
Goll  {x),  due  to  destruction  of  the  posterior  column  {x)  by  extension 
of  the  cavity  seen  in  Figure  3. 

Fig.  4. — Syringomyelia  and  3Iultiple  Sclerosis.  In  addition  to  the 
cavity  formation  there  are  extensive  sclerotic  areas  in  the  anterolateral 
and  posterior  columns,  where  the  mediillary  sheaths  of  the  fibers  have 
been  destroyed.     The  diseased  portion,  therefore,  appears  white. 

Ah}>reviations. — ca.  Anterior  horn;  ch,  direct  cerebellar  tract;  cc^ 
central  canal  (or,  more  accurately,  cavity);  /«,  fl^  fp,  anterior,  lateral, 
and  posterior  columns;  fB,  fG,  columns  of  Burdach  and  Goll. 


Tab.  76. 


Fig.l. 


Fig.  2. 


Fig.  3. 


Tab.  77. 


Fig.  1. 


Fig.  3. 


Fig.  2. 


Fig.  4. 


PLATE  77. 
Multiple  Cerebrospinal  Sclerosis. 

A  woman  twenty -five  years  of  age  had  for  several  months 
noticed  increasing  weakness  of  the  hands,  with  tremors  and 
inability  to  grasp  objects  (intention  tremor).  Later  there 
were  added  stiff,  uncertain  gait,  nystagmus,  scanning 
speech,  optic-nerve  atrophy  (wliite,  pale  fundus),  and  ex- 
aggeration of  the  reflexes.  Sensation  was  normal;  slight 
vesical  disturbance.  In  the  course  of  three  years  the 
woman  became  completely  bedridden  and  finally  died  of 
pneumonia. 

Autopsy. — Irregularly  scattered  sclerotic  foci  in  the  brain 
and  spinal  cord,  where  the  medullary  sheaths  of  the  nerve- 
fibers  were  partially  destroyed.  The  axis-cylinders  in  some 
parts  were  i)reserved. 

Fig.  1. — Longitudinal  Section  through  the  Thoracic  Region^ 
showing  a  Sclerotic  Focus  (/)  in  the  Posterior  Columns,  lohich 
are  included  in  the  Section. 

Figs.  2  and  4. — Cross-sections  through  the  Thoracic  Region. 
In  Figure  2  almost  the  entire  cross-section  is  involved,  a 
portion  of  the  anterolateral  columns  alone  being  preserved; 
all  of  the  gray  matter  of  the  anterior  and  posterior  horns  is 
involved. 

Figure  4  shows  a  smaller  focus  (/)  in  the  posterior  col- 
umns and  in  the  posterior  and  anterior  horns,  especially  of 
the  left  side. 

Fig.  3. — Section  through  the  Cortex  of  the  Cerebral  Hemi- 
spheres. The  radiating  fibers  of  the  white  matter  (rad) 
contain  two  small  sclerotic  foci  (x). 

Similar  foci  were  also  found  in  the  brain-stem,  the  pons, 
the  medulla  oblongata,  etc. 

Abbreviations. — m.  Anterior  horn;  cb,  direct  cerebellar 
tract;  cc,  central  canal;  cp,  posterior  horn;  fal,  anterolat- 
eral column;  fl,  lateral  column;  fp,  posterior  column;  Pyl, 
lateral  pyramidal  tract. 


PLATE  78. 

Fig,  1. — Section  through  the  Medulla  Oblongata  from  a  case  of 
Chronic  Bulbar  Paralysis  with  Amyotrophic  Lateral  Sclerosis.  A  man 
thirty-six  years  of  age  developed  a  slo^vly  progressing  atrophy  and 
paralysis  of  the  small  muscles  of  both  hands;  soon  a  marked  dis- 
turbance in  the  speech  ( bulbar  speech )  made  its  ^ip])eaiance.  The 
movements  of  the  tongue  and  lips  became  slower,  the  corresponding 
muscles  atrophied,  and  marked  fibrillary  contractions  appeared  in  the 
tongue.  The  patient's  gait  also  became  stiff  and  labored.  At  the  end 
of  two  years  there  were  complete  atrophy  and  paralysis  of  tlie  tongue 
and  lips  and  of  the  muscles  of  deglutition.  Speech  liad  become  im- 
possible. The  arms  were  completely  atrophied,  and  the  legs  spastic 
and  paralyzed.     Death  from  inspiration  pneumonia. 

The  preparation  shows  marked  destruction  of  the  cells  and  fibers  in 
the  nucleus  of  the  hypoglossus  {XII)]  light  spots  in  the  pyramids 
(Py).  Many  of  the  cells  in  the  nucleus  of  the  facial  nerve  were  also 
destroyed.     L,  Fillet;  ol,  olive;  Cr,  restiform  body. 

Fig.  2. — Section  through  the  Lower  Cervical  Cord  in  Amyotrophic 
Lateral  Sclerosis.  The  clinical  course  was  quite  similar  to  that  which 
has  just  been  described,  except  for  the  absence  of  bulbar  symptoms  in 
the  uncomplicated  form.  Thus  we  have  slowl}^  increasing  degenera- 
tion, muscular  atrophy  of  the  upper  extremities,  beginning  in  the 
thenar  and  interossei  muscles,  and  spastic  paralysis  of  the  leg-s.  Sen- 
sation and  vesical  function  are  not  affected.  The  reflexes  are  increased. 
The  specimen  shows  wide-spread  destruction  of  cells  and  fibers  in  the 
anterior  horn  (Ca),  which  is  much  reduced  in  size.  The  pyramidal 
tracts  on  both  ddes  are  degenerated. 

Fig.  3. — Section  through  the  Anterior  Horn  of  the  Certical  Cord  in 
Spinal  Muscular  Atrophy.  (Professor  v.  Striimpell's  case.)  A  man 
thirty-five  years  of  age,  the  subject  of  an  hereditary  disease,  developed 
atrophy  and  paralysis  of  the  thenar  and  interossei  muscles.  In  the 
course  of  a  year  the  atrophy  extended  to  all  the  muscles  of  the  arms, 
of  the  shoulder-girdle,  and  to  the  costal  and  nuchal  muscles.  The 
muscles  showed  fibrillar  contractions  and  the  reaction  of  degeneration. 
Sensation  normal.  No  bulbar  phenomena.  No  disturbance  of  the 
gait. 

In  the  preparation  we  see  that  the  anterior  horn  (cornu  a)  is  much 
shrunken :  extensive  destruction  of  cells.  The  anterior  roots  are  also 
very  atrophic.  (Compare  with  Plate  52,  Fig.  1.)  In  the  anterior 
horn  we  see  a  dense  network  of  cicatricial  neurogliar  tissue.  The 
lateral  column  is  normal.  B,  Column  of  Burdach;  ca,  anterior  com- 
missure; fa,  fal,  anterior  and  lateral  columns;  G,  column  of  Goll; 
Py,  lateral  pyramidal  tract. 


Tab.  78. 


^       Fig.l. 


Fig.  2. 


Fig.  3. 


Tab.  79. 


Fig.  1. 


,    Fig.  3. 


^i^ 


PLATE  79. 
Tabes  Dorsalis  (Thoracic  and  Lumbar  Portions). 

In  tabes  the  nerve-fibers  of  a  part  of  the  peripheral  sensory  neuron 
degenerate.  Usually  those  of  the  lower  extremity  are  affected;  more 
rarely  those  of  the  arm  and  of  the  face  (fifth  nerve).  Tlie  primary  seat 
of  the  disease  is  not  yet  definitely  known  (neuron  cells  in  the  spinal 
ganglia?).  It  is  probable  that  certain  reflex  paths  (collaterals  from 
the  posterior  roots)  are  the  first  to  become  diseased,  then  the  posterior 
roots  (see  Plate  83,  Fig.  5,  for  their  coui-se),  both  the  short  fibers  which 
enter  the  columns  of  Clarke  in  the  posterior  horn  and  the  long  fibers 
which  enter  through  the  lumbar  roots  and  ascend  in  the  columns  of 
Goll;  the  peripheral  portions  of  the  neuron,  the  sensory  cutaneous 
nerves,  are  always  involved  in  the  degenerative  process. 

Fig.  1. — Section  through  the  Lower  Thoracic  Region.  The  posterior 
columns  [fp)  are  very  much  paler  than  normal;  the  greater  part  of 
the  ascending  and  descending  fibers  from  the  posterior  roots  contained 
in  the  posterior  columns  is  degenerated.  The  ventral  portion  [v)  of 
the  posterior  columns  is  not  derived  from  the  posterior  roots,  and  it 
regularly  escapes  in  tabes.  The  short  tracts  which  enter  the  posterior 
horn  from  the  jiosterior  columns  at  r  are  also  entirely  destroyed  (com- 
pare the  normal  section,  Plate  49,  Fig.  1).  Owing  to  the  destruction 
of  the  fibers,  the  columns  of  Clarke  {CI)  appear  as  broad,  round,  sharply 
circumscribed  areas. 

Fig.  2. — Section  through  the  Upper  Lumbar  Region  from  another 
case.  The  degeneration  is  confined  to  symmetrical  areas  {d)  \ja.  both 
posterior  colunuis,  separated  by  a  small  area  (oval  outline,  fa)  of 
intact  tissue.  There  is  also  a  so-called  "  marginal  degeneration,"  or 
degeneration  of  the  short  tracts  w^hich  ascend  and  descend  in  the 
marginal  portions  of  the  anterior  {fol)  and  lateral  columns,  being 
derived  from  cells  in  the  gray  matter  (central  neuron).  C6,  Cerebellar 
tract;  cp,  posterior  horn;  r,  absent  radii. 

Fig.  3. — Section  through  the  Lawer  Lumbar  Region  from  a  third  case. 
In  addition  to  the  uniform  degenerated  area  in  the  posterior  cords 
(B),  the  ventral  aspect  being  normal,  we  recognize  degeneration  of  the 
posterior  roots  (r.p),  the  anterior  roots  (r.  a)  presenting  the  normal 
black  color.     Ca,  cp,  Anterior  and  posterior  horns. 


PLATE  80. 
Tabes  Dorsalis  (Cervical  Region). 

Fig.  1. — Section  through  the  Cerrieal  Spinal  Cord.  (From  case  on 
Plate  79,  Fig.  1.)  The  column  of  Goll  {/(t),  which  represents  the  con- 
tinuation of  the  long  ascending  posterior  root-fiJ)ers  of  the  lumbar  cord, 
is  completely  degenerated.  The  columns  of  Burdach  {fB)  also  present 
a  central  light  area  (long  fillers  from  the  thoracic  and  cervical  roots). 
The  zone  of  Lissauer  (L),  at  the  tip  of  the  posterior  horn,  which  con- 
tains the  outermost  root-fibers  of  small  caliber,  is  also  degenerated. 
Bp,  Posterior  roots;  r,  radii. 

The  specimens  were  taken  from  a  man,  aged  fifty,  who  for  six  years 
had  been  suffering  from  a  distressing  sense  of  pressure  in  the  epigastric 
region,  which  later  developed  into  a  typicid  girdle-pain  extending 
around  the  entire  body.  During  the  last  four  years  his  gait  became 
gradually  more  uncertain,  and  neuralgic  pains  frequently  appeared  in 
the  legs  (lancinating  pains).  Paresthesia  was  present.  The  pupillary 
and  patellar  reflexes  were  abolished.  There  were  marked  ataxia  and 
distinct  disturbance  of  sensation  in  the  legs  (delayed  pain-sense). 
Disturbance  of  vesical  function.  Later  a  chronic  effusion  developed 
in  the  left  knee-joint  (arthropathia  tabetica).  The  knee  was  flexed, 
and  the  ataxia  became  so  great  that  the  patient  had  to  keep  his  bed 
altogether. 

Fig.  2. — Section  through  the  Cervical  Region  in  so-called  ^^  High 
Tabes.''''  The  peripheral  sensory  neurons  of  the  upper,  as  well  as  of  the 
lower,  extremities  are  diseased,  so  that  almost  the  entire  posterior 
column  in  the  cervical  region  is  degenerated  (column  of  Goll,  i^Gr,  and 
of  Burdach,  FB).  In  addition  there  is  a  slight  symmetrical  affection  of 
the  pyramidal  lateral  tract  {Fy)  (the  color  is  faint) .  We  therefore  have 
a  combined  form  of  tabes. 

Fig.  3. — Section  through  the  Highest  Portion  of  the  Cervical  Cord 
{Tabes  Combine  ).  This  is  another  case  of  "  high  tabes  "  in  which  only 
a  small  portion  of  the  posterior  columns  (B,  G),  corresponding  to  the 
posterior  external  segment,  is  preserved.  There  is  also  a  plainly 
marked  degeneration  of  the  direct  cerebellar  tract  (Cb)  on  both  sides 
(tabes  combine).  The  most  pronounced  clinical  symptom  in  this  case 
was  muscular  paresis,  and  the  pupillary  reflex  was  preserved  (!). 
Hence  a  provisional  diagnosis  of  "pseudotabes "  was  made. 


Tab.  80. 


Fig.  1. 


Fig.S. 


Tab.  81. 


PLATE  81. 
Spastic  Spinal  Paralysis. 

A  woman  sixty-three  years  of  age  had  noticed  for  the 
last  two  years  increasing  weakness  of  the  arms  and  legs. 
The  paresis  gradually  went  on  to  complete  paralysis  of  the 
arms  and  legs;  the  muscles  became  rigid  and  offered  a  slight 
spastic  resistance  to  passive  mov^ements.  The  knee-jerks 
were  increased.  There  was  no  muscular  atrophy  and  no 
disturbance  of  sensation  or  vesical  function.  Finally,  after 
three  years,  there  develoi)ed  complete  paralysis  of  all  the 
voluntary  muscles  of  the  skeleton — the  muscles  of  the  eye, 
face,  pharynx,  tongue,  back  of  the  neck,  arm,  trunk,  and 
leg;  everything  else  was  normal.  Anatomicall}^  a  sym- 
metrical degeneration  of  the  entire  pyramidal  tract,  from  the 
cortex  through  the  internal  capsule,  brain-stem,  medulla 
oblongata,  and  spinal  cord  (central  motor  neuron  complex), 
was  found. 

Fig.  1. — Section  through  the  Medulla  Oblongata.  Botli 
pyramids  (Py)  are  degenerated  and  pale  in  color.  A  large 
portion  of  the  nerve-fibers  is  destroyed.  /,  Posterior  lon- 
gitudinal bundle;  L,  fillet;  ol,  olive;  V c,  descending  root 
of  the  trigeminus. 

Fig.  2. — Section  through  the  Cervical  Cord.  Bilateral  de- 
generation of  the  lateral  pyramidal  tract  (Py)  with  slight 
atrophy  of  the  walls  in  the  anterior  horn.  This  slightly 
resembles  amyotrophic  lateral  sclerosis. 

Fig.  3. — Sections  through  the  Middle  of  the  Thorjacic  Cord. 
Degeneration  of  the  lateral  pyramidal  tract  (P?/). 

Fig.  4. — Sections  through  the  Lumbar  Cord.  The  diseased 
pyramidal  tract  {Py)  has  gained  the  periphery. 


PLATE  82. 
Combined  System  Disease. 

There  are  other  cases  besides  combined  tabes  in  which, 
instead  of  one  neuron  complex,  forming  an  anatomic  and 
physiologic  unit,  becoming  diseased,  several  different  neu- 
ron complexes  are  attacked  at  the  same  time  by  a  primary 
degeneration.  It  is  not  as  yet  definitely  known  where  the 
degenerative  process  begins  in  these  cases:  whether  the 
neuron  cell  or  the  neuron-fiber  becomes  primarily  dis- 
eased. The  clinical  course  consists  in  a  slowly  progress- 
ive spastic  paresis  and  ataxia  of  the  legs  and  amis,  with 
more  or  less  pronounced  disturbances  of  sensation  and 
vesical  function.  No  muscular  atrophy.  A  similar  dis- 
ease forms  the  foundation  of  hereditary  ataxia.  (See 
text. )  The  following  sections  were  taken  from  the  spinal 
cord  in  a  case  of  this  kind: 

Fig.  1. — Section  through  the  Cervical  Cord.  A  symmetrical 
disease  of  the  lateral  (Py)  and  anterior  (Pi/d)  pyramidal 
tracts,  of  the  direct  cerebellar  tract  (Ch),  columns  of  Goll 
(fG),  and  the  central  portion  of  the  columns  of  Burdach 
ifB). 

Fig.  2. — Section  through  the  Lower  Thoracic  Cord.  The 
same  as  Figure  1.  In  the  posterior  column  the  degener- 
ation is  less  marked  and  is  confined  to  the  central  portion. 
Pya,  Cb,  Py,  as  above. 

Fig.  3. — Section  through  the  Lurahar  Cord.  The  lateral 
pyramidal  tracts  (P)  still  exhibit  marked  degeneration;  in 
the  posterior  column  {f'p)  there  is  only  a  narrow  area  of 
degeneration. 


Tab.  82. 


Tab.  83. 


.•   #    -*  ••       •       «  •  - 


PLATE  83. 
Degenerations  of  the  Peripheral  Nerves. 

Fig.  1. — Ascending  Secondary  Degeneration  of  the  Sciatic  Nerre  after 
Amputation  of  the  Leg.  A  high  amputation  of  the  leg  had  been  per- 
formed on  a  man  fourteen  years  before.  The  figure  shows  the  margin 
of  a  nerve  bundle  in  which  the  greater  part  of  the  nerve-fibers  is  de- 
stroyed. The  coarser  fibers  especially  show  a  marked  secondary 
ascending  degeneration,  due  to  the  primary  disease  in  the  neuron  cells 
situated  in  the  lumbar  cord,  caused  by  the  loss  of  function.  The 
smaller  fibers  are  better  preserved.  (Compare  the  normal  cross-section, 
Plate  51,  Fig.  3. ) 

Fig.  2. — Descending  Degeneration  of  the  Right  Optic  Nerve  after 
Destruction  of  the  Left  Later  at  Geniculate  Body  and  the  Left  Anterior 
Corpus  Quadrigeminum.  The  optic  nerves  contain  fibers  whose  neuron 
cells  are  situated  for  the  most  part  in  the  retina,  and,  in  addition, 
fibers  which  have  their  cells  in  the  above-named  subcortical  optical 
centers.  The  latter,  therefore,  undergo  descending,  the  former  ascend- 
ing, degeneration.  We  see  in  this  section  a  degenerated  area  {x)  in 
the  form  of  a  sector.  (Compare  the  normal  optic  nerve,  Plate  51.) 
V,  Sheath  of  the  optic  nerve. 

Fig.  3. — Compression  Neuritis  of  the  Optic  Nerve.  In  a  patient  suf- 
fering from  acromegaly  a  malignant  tumor  of  the  pituitary  gland, 
which  surrounded  the  optic  nerve,  led  to  partial  degeneration  {x,  x) . 
V,  Sheath  of  the  optic  nerve  (dural  sheath). 

Fig.  4. — Motor  Nerve  Bminch  in  Spinal  Muscular  Atrophy.  Note  the 
marked,  wide-spread  destruction  of  fibers,  (Belonging  to  case  shown 
on  Plate  78,  Fig.  3.) 

Fig.  5. — Posterior  Boot  From  the  Lumbar  Cord  in  Tabes  Dorsalis. 
(From  the  case  shown  on  Plate  79,  Fig.  3. )  The  anterior  bundle  {x)  of 
posterior  roots  contains  scarcely  more  than  ten  normal  fibers.  To  the 
right  of  it  there  is  another  in  a  somewhat  better  state  of  preservation. 
F,  Blood-vessels. 

Fig.  6.— Bundle  From  the  Peroneal  {External  Popliteal )  Nerve  in  Neu- 
rotic 3Tuscular  Atrophy.  Note  the  irregular  distribution  of  the  areas  of 
fiber  degeneration,  especially  in  the  central  portions  of  the  bundle. 
The  spinal  cord  is  probably  also  involved  (motor  cells  in  the  anterior 
born). 


PLATE  84. 
Multiple  Neuritis. 

Figs.  1  and  2. — From  a  cane  of  grave  Alcoholic  Polyneuritis.  (Fig. 
1  from  the  crural  nerve;  Fig.  2  from  the  sciatic  nerve.) 

A  heavy  drinker,  forty  years  of  age,  rather  suddenly  developed  an  in- 
creasing weakness  of  the  legs  which  rapidly  went  on  to  complete  paral- 
ysis. There  was  marked  tenderness,  the  patellar  reflexes  were  abol- 
ished, sensory  disturbances  were  present,  and  muscular  atrophy  devel- 
oped. His  condition  became  worse  after  injections  of  strychnin. 
The  arms  also  became  involved;  the  irregular  disturbances  persisted. 
Death  after  two  and  a  half  months. 

Marked  destruction  of  fibers  is  seen  in  all  the  peripheral  nerves. 
Some  bundles  contain  scarcely  more  than  six  to  ten  normal  fibers. 
(Compare  Plate  51,  Fig.  2.)  The  degeneration  extends  as  far  as  the 
roots  in  the  spinal  cord. 

Fig.  5. — Transverse  Section  of  the  Cervical  Cord  from  the  same  case. 
The  atrophy  of  the  anterior  roots  (r.  a),  which  traverse  the  anterolateral 
colunni,  is  plainly  seen.  There  is  also  a  well-marked  degenerated  area 
in  the  mesial  portion  (m.)  of  the  anterior  horn,  due  to  the  degeneration 
of  the  anterior  roots  which  enter  at  this  point.  There  is  a  slight 
anterior  degeneration  in  the  column  of  Goll  (long  fibers  of  the  poste- 
rior roots,  r.  p) . 

Fig.  3. — Postdiphtheric  Neuritis.  Transverse  section  through  a 
bundle  from  the  crural  nerve,  showing  advanced  degree  of  degeneration 
of  the  fibers,  from  a  boy  fifteen  years  old  who,  after  recovering  from 
pharyngeal  diphtheria,  was  suddenly  seized  with  paralysis  of  the 
pharyngeal  muscles  and  progressive  paralysis  of  the  legs.  The  knee- 
jerks  disappeared  within  ten  days.  There  was  little  pain  and  only 
slight  disturbance  of  sensibility.     Death  from  paralysis  of  the  vagus. 

Fig.  4. — Longitudinal  Section  through  a  Nerve  Bundle  from  the  Sci- 
atic Nerve.,  from  a  case  of  Infectious  3Iultiple  Neuritis  {Landry^ s  Paral- 
ysis). The  products  of  disintegration  (myelin  granules)  of  a  part  of 
the  degenerated  nerve-fibers  are  still  visible.  The  nerve-fibers  are  seen 
in  all  stages  of  degeneration. 

The  specimen  is  taken  from  a  case  in  which  the  etiology  remained 
doubtful.  A  woman  thirty  years  of  age  who  had  probably  had  a  severe 
acute  disease  (fever  ? )  presented  complete  paralysis,  first  of  the  legs 
and  then  of  the  arms  (ascending  paralysis).  The  patient  was  in  a  very 
low  condition  and  almost  unconscious  when  she  came  under  medi- 
cal treatment,  two  days  before  her  death.  The  spinal  cord  was  not 
examined. 


Tab.  84. 


PART  I. 

MORPHOLOGY   OF   THE   NERVOUS 
SYSTEM^ 

(Plates  1  to  14.) 


The  nervous  system  of  man  consists  of — 

1.  The  central  organ,  comprising  brain  and  spinal 
cord,  and  the  peripheral  nerves  which  spring  from  them. 

2.  The  sympathetic  nervous  system,  consisting  of 
the  main  trunk  of  the  sympathetic  nerve  and  its  plexuses. 

These  two  parts  communicate  with  each  other  by  numer- 
ous nerve  paths. 

The  brain  and  the  spinal  cord  are  contained  in  the 
cranium  and  vertebral  column,  resjiectively,  and  from 
these  bony  receptacles  the  nerves  issue  into  the  soft  tissues. 
The  gangliated  cords  of  the  sympathetic  lie  on  each  side 
of,  and  anterior  to,  the  vertebral  column. 

The  brain  and  spinal  cord  are  invested  by  three  mem- 
branes, termed  the  meninges.  The  outer  of  these  is  the 
dura  mater,  a  tough,  fibrous  membrane  in  close  relation 
with  the  bone  and  performing  the  function  of  a  periosteum 
to  the  interior  of  the  skull.  It  surrounds  the  brain  and 
cord  like  a  sac,  and  furnishes  tubular  sheaths  to  the  nerves 
at  their  points  of  exit,  where  the  membrane  terminates  and 
is  attached  to  the  edges  of  the  foramina  at  the  base  of  the 
skull.  The  dura  contains  the  large  sinuses  .rhich  collect 
the  venous  blood  from  the  brain  and  empty  into  the  jugu- 
lar vein.  These  venous  sinuses  are  :  The  superior  and  the 
1  1 


2  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

inferior  falciform  (longitudinal),  the  cavernous,  petrosal, 
transverse,  etc. 

The  dura  mater  sends  processes  into  the  interior  of  the 
cerebrum.  Tlie  falx  cerebri  (processus  falciformis  major) 
occupies  the  median  sagittal  line,  being  attached  in  front  to 
the  crista  galli,  and  divides  the  upper  half  of  the  cranium 
into  two  equal  parts.  The  tentorium  occupies  a  horizontal 
plane  and  forms  the  roof  of  the  posterior  fossa  of  the  skull. 

The  dura  loosely  invests  the  brain  and  cord,  leaving  an 
interval  filled  with  lymph  which  is  known  as  the  subdural 
space. 

The  second  envelope  is  formed  by  a  delicate  membrane 
known  as  the  arachnoid.  It  is  more  intimately  adherent 
to  the  brain  than  to  the  cord ;  in  the  brain  it  bridges  over 
the  convolutions  without^  dipping  down  into  the  sulci. 
On  each  side  of  the  falx  cerebri  are  seen  the  Pacchionian 
bodies,  which  consist  of  exuberant  masses  of  connective 
tissue  derivx'd  from  the  arachnoid.  Beneath  the  arachnoid 
is  the  subarachnoid  space,  ^vhich  is  subdivided  into  numer- 
ous compartments  communicating  with  one  another  and 
containing  the  cerebrospinal  fluid. 

The  innermost  envelope  is  formed  by  the  pia  mater, 
the  term  "soft  membranes"  being  applied  to  this  mem- 
brane and  to  the  arachnoid.  The  pia  closely  invests  the 
nerve  substance  and  dips  down  into  all  the  fissures  and 
cavities  in  the  brain,  as  the  tela  choroidea  inferior.  It 
conveys  the  numerous  blood-vessels  which  supply  the 
brain  and  cord. 

The  brain  consists  of  the  two  large  cerebral  hemi= 
spheres,  the  brain-stem,  and  the  cerebellum  ;  the  direct 
continuation  of  the  brain-stem  is  the  spinal  COrd.  The 
axis  of  the  latter  is  nearly  perpendicular  to  the  ])lane  of 
the  cerebellum,  as  the  brain-stem  is  bent  at  an  angle  of 
almost  90  degrees. 

The  weight  of  the  brain  in  the  adult  is  1300  to  1400 
grams.  In  man  it  averages  1360,  in  woman  1220  ;  a 
variation  as  low  as  900  grams  is  not  considered  abnormal. 


THE  CEREBRAL  HEMISPHERES.  6 

The  two  cerebral  hemispheres  comnmnicate  only  on 
their  median  surfaces  ;  they  consist  of  a  reddish-gray  layer 
of  cortical  substance,  the  eortex  cerebri,  which  is  disposed 
on  the  surface,  and  a  central  white  77iatter,  or  medullary 
substance,  situated  under  the  cortex. 

The  surface  of  the  cortex  is  thrown  into  numerous 
vermiform  convolutions  or  gyri,  marked  off  by  fissures  or 
sulci,  an  arrangement  that  greatly  increases  the  surface 
area  of  the  brain.  The  fundamental  type  of  the  convo- 
lutions is  constant,  but  there  are  numerous  individual 
variations. 

Each  cerebral  hemisphere  is  divided  into  several  lobes, 
eacli  lobe  comprising  several  convolutions  and  a  portion 
of  the  white  matter. 

In  the  anterior  fossa  lodges  the  frontal  lobe,  which 
forms  the  anterior  pole  of  the  cerebrum  and  is  marked 
by  two  principal  fissures  (sulc.  front,  sup.  and  inf.),  which 
divide  it  into  three  convolutions  or  gyri  (gyr.  front,  sup., 
med.,  and  inf ).  The  posterior  boundary  of  the  frontal 
lobe  is  formed  by  the  central  sulcus  or  fissure  of  Rolando, 
which  commences  a  little  behind  the  middle  of  each  hemi- 
sphere and  runs  downward  and  forward.  This  fissure 
divides  the  two  ^'central  convolutions^^  (gy^*  centr.  ant. 
and  post.)  (ascending  frontal  and  ascending  parietal  con- 
volutions). 

Posterior  to  the  central  convolutions  is  the  parietal 
lobe,  which  is  divided  by  the  intraparietal  sulcus  into  the 
superior  and  inferior  parietal  lobules  (lob.  pariet.  sup. 
and  inf.). 

The  posterior  pole  of  the  brain  is  formed  by  the  occip- 
ital lobe,  which  is  contiguous  to  the  parietal.  ^  Like  the 
frontal  lobe,  it  is  divided  into  three  convolutions  (gyr. 
occip.  med.,  sup.,  and  inf.) ;  the  under  surface  of  the 
occipital  lobe  rests  on  the  tentorium. 

^  Occasionally  the  division  between  the  parietal  and  occipital  lobes 
is  abnormally  deep,  owing  to  the  unusual  development  of  the  so-called 
"  Simian  fissure." 


4  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

The  middle  fossa  of  the  skull  accommodates  the  tem- 
poral lobe,  which  is  subdivided  into  three  convolutions 
(gyr.  temp,  med.,  sup.,  and  inf.)  by  three  fissures  (sulc. 
temp,  sup.,  med.,  and  inf ).  In  front  and  above  it  is 
divided  from  the  frontal  lobe  and  the  central  convolutions 
by  a  broad  and  deep  sulcus,  the  fissure  of  Sylvius,  while 
it  is  directly  continuous  behind  with  the  inferior  convolu- 
tions of  the  parietal  lobe.  Hence  the  inferior  parietal 
lobule  comprises  two  convolutions,  arching  from  before 
backward,  known  as  the  supraraarginal  and  angular  gyri 
(^pli  courhe).'^ 

At  the  bottom  of  the  fissure  of  Sylvius  is  another  lobe, 
the  island  of  Reil,  with  its  small  convolutions,  covered 
over  by  the  adjoining  lobes,  especially  the  temporal  and 
central.  [Note. — More  correctly,  the  part  of  the  inferior 
frontal  convolution  in  front  of  the  ascending  limb  of  the 
fissure  of  Sylvius.]  The  convolutions  which  overlap  the 
island  are  collectively  known  as  the  operculum,,  which  is 
again  subdivided  into  the  operculum  frontale,  centrale 
(or  Rolando),  and  parietale. 

The  convolutions  hitherto  described  can  be  seen  on  the 
external  convex  surface  of  the  hemisphere.  On  the  mesial 
surface  of  the  hemispheres  the  continuation  of  the  superior 
frontal  convolution  can  be  seen.  The  central  convolutions 
run  together  in  the  paracentral  lobule^  and  the  parietal  lobe 
is  continued  as  the  precuneus.  The  latter  is  separated 
from  the  mesial  surface  of  the  occipital  lobe  by  the  parieto- 
occipital fissure.  The  mesial  surface  of  the  occipital  lobe 
is  divided  into  the  cuneus,  and  beneath  this  and  separated 
from  it  by  the  deep  calcarine  fissure,  the  lobulus  lingualis. 

On  the  under  surface  of  the  temporal  lobe  the  inferior 
temporal  joins  the  occipitotemporal  convolution,  and  to  the 
mesial  side  of  the  latter  and  separated  from  it  by  the 
occipitotemporal  fissure  is  the  inferior  marginal  convolution, 

^  Many  anatomists  count  three  convolutions,  gyrus  marginalis, 
angularis,  and  praeoccipitalis.  The  convolutions  in  this  portion  of  the 
brain  are  subject  to  frequent  variations. 


THE  CEREBRAL  HEMISPHERES.  5 

the  gyrus  hippocampi,  which  terminates  anteriorly  in  the 
uncus.  The  orbital  surface  of  the  frontal  lobe  is  marked 
by  the  following  fissures  :  1'he  sulcus  rectus  (olfactory 
sulcus)  and,  external  to  it,  the  triradiate  fissure,  which 
forms  part  of  the  middle  frontal  convolution. 

In  the  central  portion  of  the  median  surface  of  the  hemi- 
spheres, which  is  surrounded  by  the  above-mentioned 
convolutions,  the  arrangements  are  somewhat  different. 
Above,  the  cortex  ends  in  the  gyrus  fornicatus,  and  be- 
low in  the  gyrus  hippocampi  (upper  and  lower  marginal 
convolutions).  Underneath  the  upper  marginal  convolution 
the  white  matter  of  the  brain  projects  from  the  interior  of 
the  two  hemispheres  and  forms  the  corpus  callosum. 

Above  the  lower  marginal  convolution  the  white  matter 
also  projects  from  the  hemispheres,  and  converging  from 
either  side,  forms  the  crusta  (or  pes),  the  ventral  portion 
of  the  cerebral  peduncle,  which  begins  at  this  point. 

Between  the  corpus  callosum  and  the  cerebral  peduncle 
is  a  series  of  deeply  placed  structures  and  spaces  which 
will  be  described  more  in  detail  later  on.  Thus  the  entire 
intermediate  portion,  which  is  surrounded  by  the  marginal 
convolutions,  is  not  covered  with  cortical  substance. 

The  corpus  callosum,  which  connects  tiie  two  hemi- 
spheres, forms  a  robust  layer  of  white  fibers ;  the  larger 
central  portion  is  nearly  horizontal ;  the  anterior  extremity, 
or  geiiK,  is  reflected  downward  and  then  backward  to  the 
base  of  the  brain  ;  posteriorly  it  ends  in  a  thick  rounded 
fold,  the  splenium.  The  mass  of  white  matter  in  the  inte- 
rior of  each  hemisphere  forms  the  nucleus  of  the  lobes  we 
have  described.  The  upper  half,  down  to  the  level  of  the 
corpus  callosum,  is  formed  chiefly  by  the  radiating  fibers 
of  the  corpus  callosum,  and  a  section  at  this  level  is  known 
as  the  centrum  semiovale  Vieussenii  (centrum  ovale 
majus).  The  basal  portion  contains  in  its  substance  a 
grayish-red  mass  the  size  of  a  goose's  egg, — the  corjws 
striatum, — which  is  divided  into  the  lemiicular  nucleus,  or 
lateral  portion,  and  the  caudate  nucleus,  or  mesial  portion. 


b  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

These  two  parts  are  divided  by  the  layer  of  white  fibers 
whicli  we  have  already  described  as  emerging  from  the 
base  of  each  hemisphere — namely,  the  ventral  portion  of 
the  cerebral  peduncle,  or  crusta  pedunculi. 

In  the  interior  of  each  hemisphere  is  a  system  of  cavi- 
ties filled  with  lymph — the  ventricles.  The  roof  of  the 
lateral  ventricle  is  formed  by  the  centrum  ovale,  which  is, 
therefore,  also  called  the  tegmentum  ventriculorum. 

The  free  upper  surface  of  the  corpus  striatum  projects 
from  the  white  matter  and  bulges  from  without  and  below 
into  the  lateral  ventricle. 

This  portion  of  the  lateral  ventricle,  which  lies  between 
the  lateral  portion  of  the  corpus  callosum  and  the  surface 
of  the  corpus  striatum,  is  known  as  the  cella  media  (body 
of  the  lateral  ventricle).  The  ventricle  is  continued  into 
the  frontal  lobe  as  the  anterior  horn,  and  into  the  occipital 
lobe  as  the  posterior  horn,  while  the  descending  horn  dips 
down  into  the  temporal  lobe.  The  anterior  and  posterior 
horns  are  surrounded  on  every  side  by  white  matter,  and 
thus  lie  buried  in  the  wOiite  matter  of  the  hemispheres. 
The  descending  horn,  on  the  contrary,  is  open  toward  the 
median  line,  the  opening  being  effected  by  a  reflection  on 
itself  of  the  lower  marginal  convolution,  the  gyrus  hipjio- 
campi,  which  therefore  projects  into  the  descending  horn 
and  forms  a  thick  rounded  fold,  the  cornu  ammonis. 
The  free  edge  of  the  cortical  layer  of  the  gyrus  hippo- 
campi is  really  formed  by  the  narrow  gyrus  dentatus 
(fascia  dentata  or  fascia  Tarini).  This  arrangement  is 
clearly  seen  in  Figure  1. 

At  the  free  border  of  the  cornu  ammonis  is  the  begin- 
ning of  the  fimbria,  or  terminal  portion  of  the  white  mat- 
ter belonging  to  the  gyrus  hippocampi,  or,  more  specifi- 
cally, of  the  gyrus  dentatus.  The  fimbria  passes  backward 
and  upward  from  the  anterior  extremity  of  the  descending 
horn,  along  with  the  superficial  corrugated  portion  of  the 
cornu  ammonis  (digitationes  cornu  ammonis).  At  the  junc- 
tion of  the  descending  horn  with  the  cella  media  the  fimbria 


THE  CEREBRAL  HEMISPHERES.  7 

leaves  the  corim  ammonis  and,  joining  with  that  of  the  op- 
posite side,  forms  the  ascending  limb  of  the  fornix  (crus  as- 
cendens  fornicis)  and  unites  with  the  lower  posterior  seg- 
ment of  the  corpus  callosum  in  the  central  triangular  inter- 
val, known  as  the  lyra.  The  fornix  (or  ''  cortical  medulla  " 


Fig.  1. — Section  through  the  lower  marginal  convolution  (medul- 
lary sheath  stain):  «,  Aiveus;  c.  Am^  cornu  ammonis;  F.  I,  fascicul. 
longitud.  inf.;  Fo,  fornix;  g.  d,  gyrus  den tatus;  gyr.  Hippoc,  Hippo- 
campal  gyrus;  gyr.  o.  t,  occipitotemporalis;  Zi,  hiius  of  gyr.  dentat. ; 
/.  i,  lamina  med.  involuta  (tangential  fibers);  n.  c,  caudate  nucleus 
(tailpiece) ;  i>/,  plexus  choroid,  inf.;  st.  I,  stratum  lacunosum;  sub, 
subiculuni;  tap,  tapetum;  t.  m,  taenia  medullar. ;  v.  inf.,  inferior  ven- 
tricle (descending  cornu). 


of  the  hemisphere)  passes  along  the  under  surface  of  the 
corpus  callosum,  with  which  it  is  united,  to  a  point  just 
behind  the  genu,  where  it  leaves  the  corpus  callosum  and 
again  takes  a  downward  course,  after  dividing  into  the  two 
descending  limbs  or  anterior  pillars  of  the  fornix  (crura 
descend,  fornicis).     At  the  base  of  the  brain  the  anterior 


8 


MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 


pillars  of  the  fornix  are  reflected  backward  and  end  in  the 
corpora  albicantia. 

It  follows  that  between  the  genu  of  the  corpus  callosum 
and  the  anterior  pillars  of  the  fornix  there  remains  an  open 
space  which  is  occupied  by  two  slender  folds,  the  septum 
lucidum,  bounding  a  small  cavity,  the  ventricle  of  the 
septum  lucidum  {fifth  ventnde).     To  either  side  of  each 


Fig.  2. — Schema  of  the  ventricles  of  the  brain  (coronal  section): 
PI.  ch.  Plexus  choroideus  lateralis  ;  tel.,  tela  choroidea  ;  m,  plexus 


choroidea  med. 
missure). 


o,  membrana  obturatoria  ventr.  III.  (anterior  com- 


septum  and  underneath  the  corpus  callosum  is  the  lateral 
ventricle. 

In  the  floor  of  the  lateral  ventricles,  therefore,  the  sur- 
face of  the  corpus  striatum  is  seen  projecting  from  the 
white  matter  of  the  hemispheres.  The  broadest  anterior 
portion,  which  lies  toward  the  anterior  horn,  is  known  as 
the  caput,  or  head  of  the  corpus  striatum,  or  in  transverse 
section  as  the  caudate  nucleus.     From  the  caput  it  runs 


THE  CEREBRAL  HEMISPHERES.  9 

backward  and  downward  and  forms  the  narrow  tall,  which, 
at  the  junction  of  the  descending  horn  with  the  body, 
sweeps  downward  and  finally  forward  to  form  part  of  the 
roof  of  the  descending  horn. 

To  the  mesial  side  of  the  corpus  striatum  and  parallel 
with  it  is  a  narrow  band  of  white  fibers,  the  lamina  cor- 
nea, which  contains  a  large  vein.  It  separates  the  corpus 
striatum  from  a  large  structure,  the  optic  thalamus,  which 
lies  to  its  mesial  and  posterior  side  and  presents,  in  trans- 
verse section,  a  grayish-red  mass  similar  to  that  of  the 
corpus  striatum.  At  the  base  of  the  brain  the  optic 
thalami  gradually  approach  each  other  and  the  median 
line  ;  the  cavity  betw^een  them  is  known  as  the  third  (or 
middle)  ventricle.  The  bodies  of  the  lateral  ventricles 
directly  communicate  with  the  third  ventricle  by  means 
of  the  foramina  of  Monro,  two  slit-like  apertures  situated 
immediately  behind  the  anterior  pillars  of  the  fornix. 

The  roof  of  the  third  ventricle  would  be  formed  by  the 
fornix  and  superimposed  corpus  callosum  w^ere  it  not  for 
the  fact  that  a  process  of  the  pia  mater  passes  under  the 
splenium  of  the  corpus  callosum  (great  transverse  fissure) 
and  penetrates  into  the  third  ventricle,  which  is  open  at 
this  point.  This  vascular  prolongation  of  the  pia  spreads 
out  under  the  fornix  in  a  thin  layer  (velum  interpositum) 
Avhich  forms  the  roof  of  the  third  ventricle,  and  is  known 
as  the  tela  choroidea  sui>erior.  It  contains  at  its  center 
two  cord-like  granular  structures,  the  choroid  plexuses 
(plex.  choroidei  med.),  which  pass  from  the  third  to  the 
lateral  ventricles  in  the  foramen  Monro  as  plexus  cho- 
roideus  lateralis  (the  choroid  plexuses  of  the  third  ven- 
tricle). Here  they  are  closely  applied  to  the  lateral  border 
of  the  optic  thalamus,  and,  passing  backward,  finally  enter 
the  descending  horn,  where  they  become  continuous  with 
the  pia  mater,  which  enters  through  the  foramen  of 
Monro. 

As  has  been  stated,  the  white  matter  is  encroached  upon 
in  the  central  portion  of  each  hemisphere  by  the   gray 


10  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

masses  of  the  corpus  striatum  and  optic  thalamus,  which 
increase  more  and  more  in  size  as  the  base  of  the  brain  is 
approached.  The  white  fibers  as  they  descend  from  the 
centrum  semiovale  pierce  the  corpus  striatum  and  form 
the  anterior  limbs  of  the  internal  capsule  (capsula  Reilii), 
dividing  the  lateral  portion  or  lenticular  nucleus  from  the 
caudate  nucleus.  Another  bundle  of  white  fibers  passes 
downward  as  the  posterior  limb  of  the  internal  capsule, 
and  separates  the  lenticular  nucleus  from  the  optic  thal- 
amus. The  anterior  and  posterior  limbs  unite  to  form  the 
genu  of  the  internal  capsules.  Part  of  the  fibers  of  the 
internal  capsule  enter  the  corpus  striatum  and  optic  thal- 
amus and  disappear  in  these  structures  ;  others  are  con- 
tinued downward  toward  the  base  of  the  brain,  where  they 
emerge  in  the  foi'm  of  the  above-mentioned  cimsta  or  pes. 

The  lenticular  nucleus,  which  is  wedged  in  between  the 
internal  capsule  and  the  island  of  Reil,  is  divided  into 
several  portions  :  a  larger  lateral  portion,  the  putamen, 
and  several  median  segments  not  related  morphologically 
to  the  putamen,  together  forming  the  globus  pallid  us. 
The  putamen  and  the  caudate  nucleus  together  really  form 
the  corpus  striatum. 

Outside  of  the  putamen  the  white  matter  of  the  hemi- 
spheres is  continued  downward  in  a  thin  layer  as  the 
external  capsule;  between  this  and  the  white  matter  of 
the  insula  (capsula  extrema)  there  is  a  narrow  strip  of 
gray  matter  running  parallel  wdth  the  insula  and  known 
as  the  claustrum. 

Below  the  lenticular  nucleus  the  white  matter,  which  at 
this  point  is  reduced,  by  the  encroachment  of  the  gray 
matter,  to  two  narrow  strips,  the  internal  and  external 
capsules,  begins  to  expand,  reaching  its  greatest  develop- 
ment posteriorly  in  the  white  matter  of  the  temporal  lobe. 
Under  the  anterior  portion  of  the  lenticular  nucleus,  em- 
bedded in  the  mass  of  white  matter  between  the  frontal 
and  temporal  lobes,  is  a  small  roundish  mass  of  gray  matter, 
the  amygdaloid  nucleus. 


THE  CEREBRAL  HEMISPHERES.  11 

The  upper  and  mesial  surface  of  the  optic  thalamus  may 
be  exposed  by  removing  the  corpus  callosum  with  the 
fornix  and  velum  interpositum.  It  presents  in  front  a 
small  prominence,  the  anterior  tubercle,  and  projects 
backward  and  outward  to  form  a  prominent  mass,  the 
pulvinar. 

The  median  surfaces  of  the  optic  thalami  form  the 
lateral  walls  of  the  third  ventricle.  Along  the  upper 
inner  margin  of  the  optic  thalami  is  seen  the  toenia  medul- 
laris,  which  ascends  from  the  interior  of  the  brain  and, 
passing  backward  in  the  form  of  the  pedunculus  conaril  (or 
stria  pinealis),  decussates  with  the  corresponding  structure 
of  the  other  side.  To  each  side  of  the  point  of  intersec- 
tion lies  the  small  ganglion  habenulce  (trigonwn  habemdoe). 
Resting  upon  the  decussation,  but  not  in  any  way  connected 
with  it,  is  found  the  pineal  gland  (epiphysis,  conarium, 
glandula  pinealis,  etc.). 

The  cavity  of  the  third  ventricle  is  traversed  by  three 
short  bundles  of  fibers  connecting  the  two  halves  of  the 
brain.  Immediately  in  front  of  the  anterior  pillars  of  the 
fornix,  near  the  floor  of  the  ventricle,  is  the  robust  white 
anterior  commissure.  In  the  middle  of  the  third  ven- 
tricle is  the  gray  or  middle  commissure,  which  is  easily 
torn,  while  immediately  below  and  in  front  of  the  decus- 
sation of  the  peduncles  of  the  pineal  body  is  the  posterior 
commissure. 

Beneath  the  optic  thalami  is  a  region  into  which  a  part 
of  the  white  fibers  from  the  lenticular  nucleus,  the  optic 
thalamus,  and  the  inner  capsule  project,  and  which  is 
known  as  the  regio  siibthalamica.  It  contains  the  oval 
corpus  subthalamicum  (subthalamic  body)  and  the  be- 
ginning of  the  red  nucleus  (nucleus  ruber),  which  extends 
further  backward  into  the  mesencephalon. 

The  third  ventricle  ends  in  front,  between  the  two 
anterior  pillars  of  the  fornix  ;  its  cavity  is  more  or  less 
funnel-shaped,  and  diminishes  in  size  toward  the  base  of 
the  brain,  where  it  is  continued  into  the  infundibulum. 


12  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

The  latter  is  closed  by  the  pituitary  body,  which  is  lodged 
in  the  sella  turcica  of  the  sphenoid  bone.  Owing  to  the 
gradual  encroachment  of  the  median  surfaces  of  the  optic 
thalami,  the  posterior  portion  of  the  ventricle  is  more 
shallow  than  the  anterior.  It  is  traversed  by  the  posterior 
commissure,  and  continued  backward  in  the  form  of  a 
narrow  canal,  the  aqueduct  of  Sylvius. 

The  lower  halves  of  the  optic  thalami  form  a  continu- 
ous mass,  but  their  upper  posterior  portions  (pulvinar)  are 
forced  apart  by  the  corpora  quadrlgemina,  which  rise  to 
the  surface  behind  the  posterior  commissure.  There  are 
two  anterior  and  two  posterior  quadrigemina.  On  each 
side  they  send  out  the  anterior  (superior)  and  jwsterior 
(inferior)  brachiciy  which  terminate  in  the  corpus  genicu- 
latum  latei'ale  (externum)  and  medialei  (internum),  between 
the  corpora  quadrigemina  and  the  pulvinar.  From  the 
substance  of  the  corpus  geniculatum  laterale  a  bundle  of 
white  fibers,  the  optic  tract,  takes  its  course  toward  the 
base  of  the  brain.  Beneath  the  corpora  quadrigemina  the 
ventricular  system  is  continued  as  the  aqueduct,  the  imme- 
diate surrounding  of  which  is  formed  by  the  gray  matter, 
which  also  covers  the  surface  of  the  optic  thalami  and 
forms  the  lining  of  the  third  ventricle. 

Beneath  the  corpora  quadrigemina  is  the  tegmentum, 
formed  by  the  union  of  the  fibers  from  the  subthalamic 
region.  Under  the  tegmentum  the  converging  crura  cere- 
bri emerge  from  the  hemispheres  and  form  the  continua- 
tion of  the  white  matter  of  the  internal  capsule  ;  underneath 
the  tegmentum  they  unite  to  form  the  crusta.  Between 
the  tegmentum  and  the  crusta  is  a  brownish,  crescentic 
mass,  the  substantia  nigra.  Behind  the  corpora  quadri- 
gemina and  covered  by  the  tentorium  is  the  cerebellum, 
occupying  the  interval  between  the  cerebral  hemispheres 
and  overlapped  by  the  occipital  lobes.  It  lies  in  the 
posterior  fossa  of  the  cranium,  and  consists  of  a  central 
portion,  the  vermiform  process  (vermis),  flanked  on  each 
side  by  the  hemispheres  of  the  cerebellum. 


THE  CEREBRAL  HE3IISPHERES. 


13 


The  cerebellum  is  conuected  with  the  corpora  quadri- 
gemina  by  the  superior  cerebellar  peduncles,  which  pass 
through  the  tegmental  region.  They  are  directly  cdnnected 
with  the  vermiform  process  of  the  cerebellum  by  means 
of  the  thin  anterior  medullary  velum  and  the  lingula. 
Underneath  the  superior  medullary  velum  forms  the  roof 
of  the  aqueduct,  which  is  bounded  on  each  side  by  the 
diverging  superior  peduncles,  and  at 
this  point  widens  out  into  the  fourth 
ventricle.  The  communications  of 
the  ventricular  system  are  shown  in 
Figure  3. 

The  floor  of  the  fourth  ventricle 
is  formed  by  the  rhomboid  fossa, 
and  beneath  it  are  found  the  struc- 
tures of  the  medulla  oblongata, 
which  correspond  to  continuations 
of  the  crura  cerebri  (tegmentum  and 
crusta). 

The  roof  of  the  fourth  ventricle 
is  formed  by  the  inferior  vermiform 
process.  The  tela  choroidea  inferior, 
a  process  of  the  pia  mater,  projects 
into  the  ventricle  from  behind. 

The  hemispheres  of  the  cerebel- 
lum, like  those  of  the  cerebrum,  con- 
sist of  a  superficial  cortex  of  gray 
matter  and  a  central  mass  of  white 
fibers.  They  are  subdivided  into  a 
great  number  of  small  convolutions, 

running  for  the  most  part  parallel  with  one  another  and 
grouped  into  lobules.  Each  lobule  communicates  by 
means  of  a  section  of  the  vermiform  process  with  the  cor- 
responding lobule  of  the  other  hemisphere. 

The  upper  surface  is  divided  into  two  lobes,  the  lob.  sup. 
ant.  and  post,  (semihinaris),  connected  by  the  superior  ver- 
miform process  (lob.  central.,  monticulus,  folia  cacuminis). 


Fig.  3. — Schema  of 
the  ventricles  (longitu- 
dinal section ) :  c.  «,  An- 
terior horn;  c.  m,  cella 
media  ;  c.  i,  descending 
horn  ;  c.  p,  posterior 
horn  of  lateral  ventri- 
cle ;  V.  Ill,  third  ven- 
tricle; A.  S,  aqueduct  of 
Sylvius  ;  V.  IV,  fourth 
ventricle  ;  c.  cent.,  cen- 
tral canal.  For  remain- 
ing letters  see  p.  12. 


14  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

On  the  under  surface,  from  before  backward,  are  the 
following  lobules  :  flocculus,  tonsilla,  lob.  cuneiform  is,  and 
lob.  inf.  post.  Communication  is  established  between  these 
lobules  by  means  of  the  inferior  vermiform  process,  the 
corresponding  portions  being  the  nodulus,  uvula,  pyramis, 
and  commissura  brevis.  In  the  interior  of  the  white 
matter  of  the  cerebellum  is  the  corpus  dentatum  cerebelli, 
and  in  the  white  matter  of  the  vermiform  process  the 
nucleus  tegmenti,  while  between  these  are  other  smaller 
masses  of  gray  matter  (embolus,  nucleus  globosus). 

Passing  forward  from  the  white  matter  of  the  cere- 
beUum  are  the  converging  superior  peduncles  that  have 
already  been  mentioned,  while  below,  two  bundles  of  white 
fibers,  the  middle  cerebellar  peduncles,  pass  backward 
around  the  crura  cerebri,  uniting  at  the  base  of  the  brain 
to  aid  in  the  formation  of  the  pons  Varolii.  Finally,  the 
inferior  cerebellar  peduncles  pass  backward  to  the  me- 
dulla oblongata  and  form  the  restiform  bodies.  The 
superior  peduncles  form  the  lateral  boundaries  of  the 
anterior  half  of  the  rhomboid  fossa,  while  the  restiform 
bodies  bound  the  posterior  half,  the  convergence  of  these 
two  bundles  of  white  fibers  giving  it  its  characteristic 
rhomboid  shape. 

The  floor  of  the  fourth  ventricle  is  covered  with  a  thin 
layer  of  gray  matter  (central  gray  matter);  the  center  is 
traversed  by  white  medullated  fibers,  the  striae  acusticse, 
which  meet  in  the  median  line  at  an  obtuse  angle.  Under- 
neath the  layer  of  gray  matter  are  the  continuations  of  the 
tegmental  structures,  while  the  succeeding  layer  is  formed 
by  the  structures  of  the  crusta  inclosed  and  surrounded  by 
the  pontine  fibers  derived  from  the  cerebellum.  In  the 
intervals  between  these  interlacing  bundles  of  fibers  are 
numerous  smaller  masses  of  gray  matter  (nuclei),  and  this 
entire  collection  of  structures,  together  with  the  nerves 
which  emerge  in  this  region,  is  included  in  the  term 
medulla  oblongata. 

At  the  base  of  the  brain  the  pyramidal  bodies,  consist- 


THE  MEDULLA    OBLONGATA.  15 

ing  of  white  matter,  emerge  at  the  inferior  border  of  the 
pons  as  the  continuations  of  the  crusta.  They  are  flanked 
laterally  by  the  olivary  bodies,  which  in  transverse  section 
appear  as  crumpled  leaves  of  gray  matter. 

Below  the  origin  of  the  pyramidal  bodies  the  floor  of 
the  fourth  ventricle  rapidly  diminishes  in  Avidth,  the  resti- 
form  bodies  converge  to  form  an  acute  angle,  and  the 
rhomboid  fossa  terminates  in  the  calamus  scriptorius. 
At  its  inferior  angle,  or  obex,  the  ventricle  occupies  a 
deeper  position  in  the  substance  of  the  medulla  oblongata, 
and,  disappearing  altogether  from  the  surface,  merges  in 
the  central  canal,  which  occupies  the  center  of  the  spinal 
cord  throughout  its  entire  extent. 

Shortly  before  their  junction  the  restiform  bodies  sepa- 
rate into  a  mesial  bundle,  the  funiculus  gracilis  (or 
funiculus  of  GoU),  and  a  lateral  bundle,  the  funiculus 
cuneatus  (or  funiculus  of  Burdach).  These  are  appar- 
ently continued  without  interruption  into  the  posterior 
columns  of  the  cord  (funiculus  posterior).  Yentrally  the 
pyramids  gradually  become  narrower  and  leave  the  sur- 
face to  enter  the  substance  of  the  medulla  oblongata, 
emerging  on  the  other  side  to  form  the  clecusmtion  of  the 
pyramids.  Below  the  decussation  the  pyramids  unite 
with  the  ventral  portion  of  the  restiform  bodies,  which 
does  not  form  part  of  the  posterior  columns,  to  form  the 
lateral  column  (funiculus  lateralis)  of  the  spinal  cord. 
The  anterior  columns  of  the  cord  are  formed  from  struc- 
tures situated  beneath  the  pyramids,  which  come  to  the 
surface  below  the  point  where  the  pyramids  disappear 
(funiculus  anterior). 

In  the  spinal  cord  the  gray  matter  is  found  in  the  cen- 
ter, grouped  about  the  central  canal,  being  the  continua- 
tion of  the  gray  matter  of  the  rhomboid  fossa.  It  consti- 
tutes the  anterior  and  posterior  horns.  Thus  in  the  cord 
the  gray  matter  and  the  ventricular  system  occupy  a 
deeper  position  and  lie  centrally,  while  the  white  matter 
occupies  the   periphery.       The    medulla  oblongata   thus 


16  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

gradually  becomes  converted  into  the  spinal  COrd — more 
specifically,  the  cervical  portion. 

Let  us  now  bestow  a  cursory  glance  on  the  base  of 
the  brain.  In  front  of  the  broad  prominence  formed 
by  the  pons  the  crura  are  seen  to  diverge,  having  be- 
tween them  the  posterior  perforated  space,  and  imme- 
diately anterior  to  the  latter  the  two  whitish  eminences 
known  as  the  corpora  albicantia.  In  front  of  these  is  the 
continuation  of  the  third  ventricle,  the  infundibulum, 
capped  by  the  pituitary  body,  occupying  the  angle  of  the 
optic  chiasm,  formed  by  the  junction  of  the  optic  tracts, 
which  unite  at  this  point  after  sweeping  around  the  crura. 

The  spinal  marrow  presents  a  cylindric,  whitish  cord 
about  as  thick  as  the  little  finger,  and  is  surrounded  by  the 
meninges;  it  is  contained  in  the  spinal  canal  and  extends 
to  the  upper  border  of  the  second  lumbar  vertebra.  It 
gradually  diminishes  in  diameter  from  above  downward, 
and  forms  two  enlargements  :  the  cervical  enlargement,  at 
the  level  of  the  fifth  or  sixth  cervical  vertebra,  and  the 
lumbar  enlargement,  at  the  level  of  the  twelfth  thoracic 
vertebra.  The  enlargements  are  produced  by  an  augmen- 
tation of  the  central  gray  substance  contained  in  the  ante- 
rior and  posterior  horns.  ^  The  portion  between  the  two 
enlargements  is  known  as  the  thoracic  cord,  and  the  ter- 
minal portion  is  designated  the  conus  meduUaris. 

The  two  anterior  columns  of  the  cord  are  separated  by 
a  deep  fissure,  the  anterior  longitudinal  sulcus,  which  con- 
veys the  blood-vessels.  Between  the  posterior  columns 
is  the  rudimentary  posterior  longitudinal  sulcus,  from 
which  the  septum  dorsalis  takes  its  origin  and  extends 
into  the  substance  of  the  cord. 

The  three  columns  of  the  cord  (anterior,  lateral,  and 
posterior)  surround  the  gray  matter  in  the  anterior  and  pos- 
terior horns,  as  has  been  previously  described.  The  col- 
umns and  horns  together  terminate  in  the  conus  medullaris, 

1  The  enlargements  correspond  to  the  situations  where  the  nerves 
supplying  the  extremities  make  their  exit  from  the  spinal  cord. 


THE  CRANIAL  NERVES.  17 

in  which  the  lateral  column  is  the  largest  and  the  anterior 
column  is  reduced  to  a  narrow  fasciculus.  In  the  terminal 
portion  of  the  cord  the  gray  matter  exceeds  in  amount 
the  white  matter,  while  the  opposite  condition  prevails  in 
the  cervical  enlargement. 

At  the  surface  of  the  brain-stem  and  spinal  cord  fibers 
from  the  white  matter  unite  to  form  larger  bundles,  which 
make  their  exit  as  the  peripheral  nerves. 

The  nerves  are  divided  into  twelve  pairs  of  cranial  and 
thirty-one  pairs  of  spinal. 

With  the  exception  of  the  fourth,  the  twelve  pairs  of 
cranial  nerves  emerge  at  the  base  of  the  brain  in  the  fol- 
lowing order  : 

1.  Olfactory  Nerve. — The  nerve  is  formed  by  the 
union  of  the  numerous  small  nervuli  olfactorii  which 
traverse  the  cribriform  plate  of  the  ethmoid  bone.  The 
fibers  enter  the  olfactory  bulb,  which  is  lodged  in  the 
straight  sulcus  at  the  base  of  the  frontal  lobe.  The 
olfactory  bulb  extends  backward  as  the  olfactory  tract,  and 
terminates  in  the  tuber  olfactorium,  which  is  situated  in 
front  of  and  a  little  laterally  from  the  chiasm.  The 
olfactory  tract  in  man  represents  a  rudimentary  portion  of 
the  brain,  which  in  some  animals  develops  into  a  lobe  of 
considerable  size  and  mass.^ 

2.  Optic  Nerve. — After  leaving  the  eyeball  the  two 
nerves  converge  and  enter  the  chiasm,  where  they  undergo 
a  partial  decussation  (the  larger  nasal  bundles  decussate). 
From  the  chiasm  the  optic  tracts  sweep  backward  over 
the  cerebral  peduncle  and  ascend  to  the  lateral  geniculate 
body,  in  which  they  apparently  disappear. 

3.  Oculomotor  Nerve. — It  takes  its  origin  beneath  the 
corpora  quadrigemina  in  numerous  bundles  of  nerve-fibers 
which,  after  traversing  the  substance  of  the  tegmentum, 
emerge  at  the  superior  border  of  the  pons  between  the 
converging  crura. 

^  It  follows  that,  like  the  optic  nerve,  it  differs  from  the  other 
peripheral  nerves. 
2 


18  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

4.  Trochlear  Nerve. — After  emerging  on  the  dorsal 
surface  behind  the  posterior  corpora  quadrigemina,  it  un- 
dergoes total  decussation  in  the  medullary  velum,  from 
which  point  it  descends  toward  the  base  of  the  brain  and, 
sweeping  over  the  crus,  takes  an  anterior  course. 

5.  Trifacial  Nerve. — It  is  formed  by  an  anterior 
motor  and  a  posterior  sensory  root,  and  emerges  jit  the 
lateral  border  of  the  pons.  The  posterior  root  forms  the 
Gasserian  ganglion,  on  the  distal  side  of  which  the  nerve 
subdivides  into  its  three  branches. 

6.  Abducens  Nerve. — Its  deep  origin  is  in  the  floor 
of  the  fourth  ventricle.  The  fibers  traverse  the  medulla 
oblongata,  and  the  two  nerves  emerge  at  the  inferior  border 
of  the  pons  to  the  outer  side  of  the  pyramids. 

7.  Facial  Nerve. — It  emerges  in  common  with  the 
following  nerve  at  the  inferior  border  of  the  pons  on  the 
outer  side  of  the  olivary  body. 

8.  Auditory  Nerve. — The  nerve  arises  by  two  roots, 
the  vestibular  nerve  (anterior  median  root)  and  the  cochlear 
nerve  (posterior  lateral  root),  and  emerges  from  the  base 
of  the  brain  in  company  with  the  facial. 

9.  Glossopharyngeal  Nerve,  and — 

10.  Pneumogastric  Nerve. — These  nerves  emerge  to- 
gether below  the  restiform  body  by  numerous  roots.  The 
glossopharyngeal  forms,  besides  other  ganglia,  the  petro- 
sal ganglion  ;  the  pneumogastric  forms  the  jugular  gan- 
glion. 

11.  Spinal  Accessory  Nerve. — It  arises  by  a  number 
of  roots  from  the  upper  portion  of  the  cervical  enlarge- 
ment and  medulla  oblongata,  and  makes  its  appearance  at 
the  lateral  column.  Its  internal  branch  joins  the  pneu- 
mogastric. 

12.  Hypoglossus  Nerve. — It  arises  between  the  pyr- 
amids and  olivary  body  by  numerous  fibers. 

The  spinal  nerves  are  divided  into  eight  cervical,  twelve 
thoracic,  five  lumbar,  five  sacral,  and  one,  or  rarely  two, 
coccygeal  pairs.     Their  "  roots "  arise  in  the  main  from 


THE  SPINAL  NERVES.  19 

the  corresponding  segments  of  the  cord — that  is,  from  the 
eight  cervical,  twelve  thoracic,  five  lumbar  segments,  etc. 
Each  nerve  arises  by  two  roots,  which  leave  the  spinal 
cord  separately.  The  anterior  motor  roots  emerge  be- 
tween the  anterior  and  lateral  columns,  while  the  posterior 
sensory  roots  leave  the  cord  between  the  lateral  column 
and  the  posterior  column.  Before  the  two  roots  become 
united  in  the  nerve  the  posterior  root  forms  a  node-like 
enlargement  —  the  intervertebral  ganglion  —  which  is 
lodged  in  the  intervertebral  foramen.  The  nerves  for  the 
neck  and  extremities  form  numerous  anastomoses  with 
each  other,  and  thus  produce  the  nervous  plexuses  (cervi- 
cal., brachial,  lumbar,  sacral,  etc^)  before  they  are  distri- 
buted to  the  soft  parts.  Strictly  speaking,  the  peripheral 
nerves  originate  in  these  plexuses.  From  this  arrangement 
it  follows  that  the  peripheral  nerves  contain  mixed  fibers 
from  the  anterior  and  posterior  roots  of  several  spinal 
segments.  (See  Plate  27.)  The  nerve-roots  for  the  lower 
extremity,  owing  to  their  high  origin  at  the  level  of  the 
first  lumbar  vertebra  (see  Plate  27),  continue  their  down- 
ward course  through  the  intervertebral  foramina  for  a 
certain  distance  before  they  make  their  exit,  at  first 
accompanying  the  conus  medullaris,  and  lower  down  form- 
ing the  Cauda  equina. 

The  gangliated  cord  of  the  sympathetic  consists  of  a 
series  of  small  ganglia  arranged  along  the  anterior  surface 
of  the  vertebral  column.  The  highest  of  these  are  the 
superior,  middle,  and  inferior  cervical  ganglia,  the  ganglia 
being  connected  with  one  another  by  slender  bundles  of 
nerve-fibers.  The  ganglia  are  joined  by  numerous  nerve- 
fibers  derived  from  the  cranial  nerves  and  from  the  spinal 
plexuses.  The  main  trunk  of  the  sympathetic  terminates 
on  the  coccyx  in  the  ganglion  impar.  The  sympathetic 
nerves,  after  emerging  from  the  main  trunk  and  its  gan- 
glia, either  follow  the  blood-vessels  or  join  the  cranial  and 
spinal  nerves  and  are  distributed  to  the  organs  which  they 
supply — namely,  all  smooth  muscle-fibers.     Many  of  them 


20  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

first  unite  to  form  plexuses  in  the  neighborhood  of  the 
viscera  (cardiac,  mesenteric,  intestinal  ganglia,  etc.). 

The  arteries  that  supply  the  brain  are  derived  from  the 
internal  carotid  and  vertebral  arteries  and  the  arterial 
circle  of  Willis,  which  is  formed  by  their  anastomoses. 
(See  Plate  5.)  The  branches  of  the  circle  of  Willis, 
which  occupy  the  pia,  are  the  following  :  Art.  corp.  callosi 
(corpus  callosum,  median  surfaces  of  the  hemispheres)  ; 
art.  fossae  Sylvii  (tissues  surrounding  the  fossa  and  basilar 


Carotisint 
if.S. 

Fig.  4.  Fig.  5. 

Figures  4  and  5  show  the  blood  supply  ;  figure  5  that  of  the  art. 
fossae  Sylvii  (A.f.S. ),  which  supplies  the  basal  ganglia  and  the  inner 
capsule  (a.l.st,  art.  lenticulostriata,  a  very  important  branch  in 
pathologic  lesions).  Figure  4  represents  a  transverse  section  of  the 
^inal  cord  with  its  blood-vessels.  Note  the  manner  in  which  the  gray 
substance  is  supplied  by  the  art.  sulci  anterior. 

ganglia)  ;  art.  choroidea  (ventricles) ;  art.  profunda  (occip- 
ital and  temporal  lobes),  etc.  The  blood-vessels  that 
supply  the  central  white  matter  of  the  brain  are  so-called 
end  vessels — that  is  to  say,  their  anastomosis  is  not  suf- 
ficient to  permit  neighboring  vessels  to  establish  collateral 
circulation.  The  cortical  arteries,  however,  which  enter 
from  the  pia  anastomose  freely  with  one  another. 

The  arteries  of  the  spinal  cord  are  derived  partly  from 
the  vertebral  arteries — art.  spinal.,  ant.  and  post. — and 


BLOOD-SUPPLY  OF  BRAIN  AND  SPINAL  CORD.       21 

partly  from  the  intercostal  arteries.  They  enter  the 
cord  from  all  directions,  but  especially  through  the  ante- 
rior longitudinal  sulcus,  and  are  also  end  vessels — that  is, 
they  end  blindly. 

The  returning  blood  from  the  brain  is  carried  by  the 
pial  veins  into  the  venous  sinuses,  which  empty  into  the 
internal  jugular  vein.  The  blood  from  the  third  ven- 
tricle is  collected  by  the  veins  of  Galen. 

The  veins  of  the  spinal  cord  anastomose  freely  with  one 
another  and  form  Breschet*s  venous  plexus,  which  sur- 
rounds the  dura  mater. 

The  lymphatic  channels  of  the  brain  and  spinal  cord 
(the  external  coat  of  the  vessel  forms  the  "  adventitious 
lymphatic  sheath")  communicate  with  the  lymph-spaces 
formed  by  the  meninges.  The  ventricles,  therefore,  are  in 
direct  communication  with  the  subarachnoid  space  and 
contain  the  cerebrospinal  fluid. 

The  nerves  of  the  pia  and  dura  are  derived  from  the 
sympathetic  system,  with  the  exception  of  some  in  the 
dura  which  are  branches  of  the  sensory  portion  of  the 
trifacial  nerve. 


PART    II. 

DEVELOPMENT  AND  STRUCTURE  OF 
THE  NERVOUS  SYSTEM^ 

(Plates  15  to  53.) 


The  central  nervous  system  is  derived  from  the  ecto- 
derm. In  the  center  of  the  germinal  area  two  ('^  medul- 
lary'')  folds  of  ectodermic  tissue  make  their  appearance, 
and  as  they  ap})roach  each  other  dip  down  to  form  the 
medullary  groove.  This  groove  is  later  converted  into 
the  medullary  canal  by  the  union  of  the  medullary  folds 
along  the  dorsal  line.  The  neuroglia,  or  sustentacular 
tissue  of  the  nervous  system,  and  the  essential  nerve  sub- 
stance are  developed  from  the  epithelial  layers  which  form 
the  lining  of  this  neural  canal.  The  meninges  and  blood- 
vessels are  derived  from  the  mesoderm. 

Laterally  and  dorsally  from  the  medullary  groove  a  row 
of  cells  (the  ganglionic  cord)  makes  its  appearance  and 
later  assumes  a  position  by  the  side  of  the  medullary  canal 
alontr  its  entire  extent.  These  masses  of  cells  are  the 
ancestors  of  the  intervertebral  ganglia  and  the  homologous 
ganglia  of  the  sensory  cranial  nerves  (olfactory,  Gasserian, 
cochlear,  jugular,  petrosal  ganglia,  etc.). 

The  nasal,  club-like  extremity  of  the  medullary  canal 
during  the  first  embryonal  month  expands  into  three 
primary  brain  vesicles,  the  first  and  the  third  of 
which  soon  subdivide  into  two  secondary  compartments  : 
The  primary  forebrain  (subdividing  into  the  forebrxtin 

22 


PRIMARY  SUBDIVISION  OF  THE  BRAIN.  23 

and  interbrain),  the  midbrain,  and  the  hindbrain  (the 
latter  subdividing  into  the  hindbrain  and  the  afterbrain) ; 
from  these  three,  or  more  correctly  five,  primary  vesicles 
the  entire  brain  is  later  developed.  The  cavity  of  the 
medullary  canal  becomes  converted  into  the  ventricular 
system,  and  the  thickened  walls  of  the  canal  and  of  the 
vesicles  eventually  form  the  structures  of  the  spinal  cord 
and  brain. 

By  the  ingrowth  of  the  falciform  process  of  the  dura, 
invaginating  the  roof  of  the  brain  vesicle  (palHum),  the 
forebrain  is  divided  into  two  lateral  halves  (primitive 
cerebral  hemispheres),  which,  by  virtue  of  their  more 
rapid  growth,  soon  overlap  all  the  other  portions  of  the 
brain.  The  thickening  of  the  walls  of  the  forebrain 
vesicle  results  in  the  formation  of  the  cortex  and  cerebral 
meduHa,  while  its  primary  cavity  is  converted  into  the 
lateral  ventricle,  into  which  the  primitive  corpus  striatum 
projects.  The  latter  eventually  unites  with  the  lateral 
wall  at  the  external  capsule,  while  the  median  surface 
remains  free  (caudate  nucleus). 

The  derivatives  of  the  lateral  wall  of  the  forebrain  are 
the  cortex  and  white  matter  of  the  convex  surfaces,  the 
outer  capsule,  the  caudate  nucleus,  and  the  putamen  of  the 
lenticular  nucleus.  The  derivatives  of  the  mesial  wall  are 
the  globus  pallidus  of  the  lenticular  nucleus,  the  lamina 
cornea,  fornix,  septum  lucidum,  and  nervi  Lancisi.  The 
internal  capsule  is -formed  later  by  union  with  the  optic 
thalanms  at  the  neural  end  plate. 

At  the  median  surface  of  the  vesicles  which  form  the 
hemispheres  the  corpus  callosum  makes  its  appearance, 
and,  bridging  over  the  median  line,  unites  with  the  cor- 
responding structure  of  the  opposite  side. 

The  earliest  fissures  and  convolutions  are  formed  between 
the  second  and  third  months  by  invaginations  of  the 
fcortex,  the  fissure  of  Sylvius  being  the  first  to  make  its 
appearance.     (See  Plate  16.) 

From  the  interbrain  are  derived  the  optic  thalami  and 


24  3I0RPH0L0GY  OF  THE  NERVOUS  SYSTEM. 

the  other  structures  surrounding  the  cavity,  which  later 
becomes  the  third  ventricle  (pituitary  body,  conarium, 
olfactory  tract,  optic  tract).  The  optic  thalamus  unites 
with  the  posterior  segment  of  the  corpus  striatum  ("  stalk" 
of  the  optic  thalamus),  the  union  being  effected  by  means 
of  cells  and  their  processes,  which  grow  out  from  the  optic 
thalamus  at  the  end  plate.     Thus  there  is  at  this  point  a 


Fig.  6. — Section  through  the  forebrain  and  midbrain  (second 
month).  On  the  left-hand  side  of  the  figure,  at  s,  is  the  primary 
cavity  of  the  cerebral  vesicle;  to  the  right,  at  s^,  is  seen  the  union 
between  the  corpus  striatum  (c.  str. )  and  optic  thalamus  (thai,  opt), 
which  forms  the  lateral  ventricle  (v.  1)  and  its  descending  coruu  (v.  i). 
pi.  ch,  Tela  choroidea;  v.  Ill,  third  ventricle;  pall,  pallium  (roof  of 
the  forebrain,  which  later  develops  into  the  cortex  and  white  matter 
of  the  hemispheres) . 

direct  communication  between  the  forebrain  and  the  inter- 
brain. 

From  the  midbrain  are  formed  the  corpora  quadri- 
gemina,  tegmentum,  and  crusta,  while  the  primitive  cavity 
forms  the  aqueduct. 

The  hindbrain  later  becomes  the  cerebellum,  and  the 
afterbrain  is  eventually  converted  into  the  medulla  ob- 
longata. 


HISTOLOGY  OF  NERVOUS  TISSUES  25 

Owing  to  the  more  rapid  growth  of  the  cerebral  vesicles, 
especially  of  the  forebrain,  the  following  flexures  are 
formed  :  In  the  afterbrain  the  cervical  flexure  (ventral) ; 
in  the  hindbrain  the  pontine,  metencephalic,  or  frontal 
flexure  (dorsal) ;  and  in  the  mid-  and  interbrain  the  ven- 
tral, posterior,  and  anterior  cranial  flexures. 

Microscopic  examination  of  the  central  nervous  sys- 
tem shows  that  it  is  composed  of  two  kinds  of  tissue, 
the  sustentacular  substance  (neuroglia)  and  the  nerve  sub- 
stance, consisting  of  cells  and  fibers  embedded  within  it. 
Both  tissues  are  derived  from  the  ectodermal  epithelial 
cells  which  line  the  neural  canal.  The  spongioblasts  pro- 
liferating within  the  central  canal  send  out  numerous  fibrils 
in  all  directions  which  unite  in  a  delicate  network  and  thus 
form  the  glia  cells  (spindle  cells,  astrocytes).  Another 
portion  of  the  epithelial  cells  in  the  neural  canal — the 
neuroblasts — develops  into  germ  cells,  which  send  out  first 
a  long,  thick  process,  and  later  numerous  smaller  arbor- 
izations from  which  the  ganglion  cells  and  nerve-fibers  are 
formed.  Aggregations  of  these  germ  cells  are  found  in 
certain  regions  of  the  central  nervous  system,  as  in  the 
entire  cortex  of  the  cerebrum  and  cerebellum  and  in  the 
basal  ganglia,  which  must  be  regarded  as  modified  por- 
tions of  the  cortex.  They  are  also  found  in  the  optic 
thalamus,  the  corpora  quadrigemina,  etc.,  and,  finally, 
below  the  midbrain,  surrounding  the  central  canal  and 
extending  down  to  the  lower  extremity  of  the  spinal  cord, 
where  they  are  collectively  t6rriied  the  central  nuclear  layer. 

The  remaining  portions  of  the  central  nervous  system 
are  formed  chiefly  by  the  long  processes  of  these  cells. 
Together  these  form  the  medullary  or  white  matter,  while 
the  cell  aggregations  represent  the  ancestors  of  the  gray 
matter. 

The  term  neuron  (rb  vedpov,  nerve  unit)  comprises  the 
nerve-cell  with  its  entire  nerve  process,  including  all  its  con- 
nections. 

The  long  processes  from  the  ganglion  cells  in  the  cere- 


26  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

bral  cortex,  basal  ganglia,  and  optic  thalami  begin  and  end 
within  the  central  organ — they  are  central  neurons.  The 
processes  from  the  cells  grouped  about  the  central  canal, 
however,  in  part  leave  the  central  organ  and  run  toward 
the  periphery  of  the  body,  or  they  originate  in  the  periph- 
eral spinal  ganglia  and  grow  into  the  central  organ — they 
are  peripheral  neurons.  The  latter  form  the  motor 
cranial  nerves,  which  grow  out  from  the  mid-  and  hind- 
brain,  and  the  motor  spinal  nerves,  which  originate  in  the 
ventral  nuclear  layer  of  the  spinal  cord  and  emerge  from 
the  anterior  horn  as  the  anterior  roots.  These  last  repre- 
sent the  long  processes  of  the  ganglion  cells  situated  in  the 
anterior  horns. 

The  development  of  the  peripheral  sensory  nerves  is  the 
exact  reverse  of  this.  They  originate  in  the  cells  of  the 
spinal  ganglia,  and  enter  the  dorsal  nuclear  layer  of  th^ 
spinal  cord  in  the  posterior  horn — sensory  spinal  nerves. 
In  the  same  way  the  sensory  cranial  nerves  originate  in  the 
Gasserian,  cochlear,  petrosal,  and, jugular  ganglia,  in  the 
retina,  and  in  the  olfactory  mucous  membrane,  which  are 
the  analogues  of  the  spinal  canal,  and  enter  the  substance 
of  the  brain  (olfactory  bulb,  midbrain,  afterbrain).  At  the 
same  time  another  peripheral  process  grows  out  from  each 
of  these  cells  and  runs  to  the  skin  as  a  peripheral 
sensory  nerve.  This  neuron,  therefore,  has  its  cell  aj)- 
proximately  in  the  middle  of  its  course.  ^ 

The  neuroblasts  gradually  become  converted  into  gan- 
glion cells,  and  their  processes  may  grow  to  a  considerable 
length — in  some  cases  to  one  meter.  About  the  fifth 
month  these  processes  become  covered  with  a  layer  of  deli- 
cate whitish  medullary  substance,  which  accompanies  the 
process  throughout  its  entire  extent — in  other  words, 
medullation  begins  to  take  place.     Every  long  process  re- 

^  We  learn  from  comparative  anatomy  that  as  we  ascend  in  the 
animal  scale  the  cell  of  the  peripheral  sensory  neuron  gradually  de- 
scends more  and  more  toward  the  spinal  ganglia  from  its  original  posi- 
tion in  the  skin. 


MEDULLATION.  27 

ceives  such  a  covering  or  medullary  sheath  and  thus  be- 
comes a  functionating  nerve-fiber. 

Medullation  occurs  at  different  times  in  the  different 
neuron  plexuses.  It  begins  during  the  fifth  fetal  month, 
as  has  been  stated,  and  continues  to  adult  life ;  successive 
portions  of  the  process  become  covered  with  the  medullary 
substance,  which  gives  them  their  characteristic  white 
color.  The  rule  is  that  those  nerve  paths  which  first 
become  functional  first  undergo  medullation.  Thus  the 
peripheral  reflex  paths  are  the  first  to  become  medullated, 
the  sensory  central  conduction  paths  before  the  motor,  the 
peripheral  paths  before  the  central,  the  projection  fibers 
before  the  association  fibers,  etc. 

Medullation  begins  in  the  fifth  embryonal  month  in  cer- 
tain portions  of  the  spinal  cord  and  brain,  which  are  most 
important  from  a  phylogenetic  point  of  view.  In  the 
hemispheres  medullation  does  not  begin  before  the  ninth 
month,  the  tegmental  radiation  connecting  the  superior 
parietal  with  tiie  posterior  central  gyrus,  and  the  optic 
radiation  being  the  first  to  become  medullated.  The  pyr- 
amidal tract  and  a  part  of  the  column  of  GoU  in  the  spinal 
column  are  nonmedullated  at  birth.  In  the  brain  medul- 
lation begins  at  birth  in  the  projection  fibers  and  continues 
to  the  third  month  (central,  occipital,  temporal,  hippo- 
campal  convolutions).  In  the  frontal  lobe  and  inferior 
portions  of  the  parietal  and  temporal  lobes  medullation 
does  not  begin  until  later  (from  the  fifth  to  the  ninth 
month). 

The  fully  formed  neuroglia  consists  of  numerous  small 
cells  (supporting  cells,  glia  cells)  the  processes  of  which 
form  a  close,  delicate  network  of  innumerable  fibrils,  in 
which  the  ganglion  cells  and  nerve-fibers  are  embedded. 
The  original  epithelial  cells  persist  as  the  ependyma,  which 
lines  the  walls  of  the  central  canal  and  ventricular  system. 

Fully  matured  ganglion  cells  consist  in  part  of  large 
cells,  which  may  have  various  forms,  but  all  possessing  a 
distinctly  marked  nucleus,  while  their  protoplasm  may  be 


28  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

variously  modified  and  is  often  the  seat  of  pigmentation  : 
in  part  of  small  cranial  cells  consisting  almost  exclusively 
of  nuclear  substance.  The  cells  send  out  processes  in  all 
directions,  some  of  which  form  a  rich  arborization  in  the 
immediate  neighborhood,  thus  increasing  the  sphere  of 
action  of  the  cell-body  (dendrons  or  protoplasmic  pro= 
cesses),  and  a  single  process  which  arises  as  the  above- 
mentioned  process  of  the  neuroblast  and  later  is  known  as 
the  axis=cylinder  process. 

After  its  exit  from  the  ganglion  cell  this  axis-cylinder 
process  becomes  medullated,  and  is  then  known  as  a  nerve- 
fiber.  The  nerve-fiber,  therefore,  consists  of  an  axial  fila- 
ment, which  in  turn  is  composed  of  numerous  single 
fibrillse  and  an  investing  medullary  sheath  arranged  in 
segments.  At  its  point  of  exit  from  the  central  organ 
the  nerve-fiber  (peripheral  nerve)  becomes  invested  by  an 
additional  delicate  envelope  outside  of  the  medullary 
sheath,  which  is  known  as  the  sheath  of  Schwann,  primi- 
tive sheath,  or  neurilemma.  The  length  of  the  axis- 
cylinder  process  varies  greatly,  but  it  always  ends  by 
splitting  up  into  terminal  fibrils,  although  it  may,  at  vari- 
ous levels,  give  off  lateral  twigs,  or  collaterals,  which  also 
break  up  into  terminal  fibrils.  Cells  provided  with  a 
long  process  (Deiters'  type)  gradually  preponderate  over 
those  whose  processes  are  short  and  break  up  into  their 
terminal  fibrils  in  the  immediate  vicinity  of  the  cell  (Golgi^s 
cells). 

The  ganglion  cell  with  its  dendrons  and  the  axis- 
cylinder  with  its  terminal  fibrils  together  form  an  anatomic 
and  physiologic  unit — a  neuron.  Every  nervous  pathway 
is  made  up  of  a  series  of  such  neurons,  communicating 
with  one  another.  There  does  not  appear  to  be  any  direct 
anatomic  continuity  in  these  neurons,  ^  which  communicate 

^  The  doctrine  of  the  neurons,  especially  the  histologic  conditions 
as  we  have  just  described  them,  has  recently  been  attacked,  with  some 
show  of  reason.  Some  observers  claim  to  have  discovered  anastomoses 
between  the  neurons,  and  axis-cylinders  taking  their  origin  in  plexuses. 


TBANS3nSSI0X  OF  NERVOUS  IMPULSES.  29 

with  one  another  very  much  like  cog-wheels,  the  terminal 
fibrils  of  the  axis-cylinder  of  one  neuron  inserting  them- 
selves between  the  arborizations  of  the  cells  (dendrons)  of 
another  neuron.  The  brain,  spinal  cord,  peripheral  nerves, 
and  sympathetic  system  are  composed  exclusively  of  neurons 
of  this  character  and  their  "  articulations/' 

The  transmission  of  an  impulse  from  one  neuron  to  an- 
other is  probably  effected  by  some  form  of  movement  in 
the  terminal  fibrils.  The  impulse  is  carried  away  from 
the  cell  in  the  axis-cylinder  and  toward  the  cell  in  the 
dendrons.  Every  neuron  probably  acts  in  relation  with 
several  others  (intermediate  neurons),  the  most  extensive 
communication  being  made  possible  by  the  innumerable 
dendrons  and  collaterals. 

The  gray  matter  of  the  nervous  system  (cortex,  gan- 
glia, basal  nuclei)  is  composed  of  the  supporting  neurog- 
liar  tissue,  the  ganglion  cells  with  their  dendrons,  and 
more  or  less  numerous  nerve-fibers,  both  medullated  and 
nonmedullated  (pale  or  Remakes  fibers). 

The  white  matter  (medulla  of  the  hemispheres,  cor- 
pus callosum,  inner  capsule,  cerebral  peduncle,  columns  of 
the  spinal  cord,  and  peripheral  nerves)  consists  of  medul- 
lated nerve-fibers  only,  the  color  and  consistency  of  the 
substance  depending  on  the  presence  of  this  medullary 
envelope. 

A  better  idea  of  the  minute  microscopic  structures  of 
the  various  portions  of  the  central  nervous  system  than  can 
be  given  by  a  mere  description  will  be  obtained  from  a 
study  of  plates  17  to  26  and  their  explanations  and  from 
the  drawings  in  the  text. 

It  now  remains  to  give  a  short  account  of  the  internal 
connections  between  the  various  portions  of  the  central 
nervous  system. 

The  fibers  which  form  the  centrum  semiovale  begin  and 

This,  however,  has  not  been  definitely  proved  in  the  case  of  man. 
The  near  future  w^ill  undoubtedly  bring  forth  many  modifications  of 
the  doctrine. 


30  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

end  in  the  cellular  layers  of  the  cortex.     They  are  divided 
into  three  systems. 

I.  The  Commissural  Fibers. — These  form  the  greater 
part  of  the  central  white  matter  of  the  corpus  callosum 
and  connect  symmetric  areas  of  the  convolutions  of  the 
two  hemispheres  with  each  other.  ^  Those  portions  of  the 
cortex  that  are  not  connected  by  the  fibers  of  the  corpus  cal- 
losum— namely,  the  inferior,  temporal,  and  occipital  convo- 
lutions, and  the  olfactory  lobe — communicate  with  one 
another  by  means  of  the  deep  anterior  commissure. 

II.  Association  Fibers. — These  are  composed  of  bundles 
of  white  fibers  connecting  the  individual  convolutions  of 
the  same  hemisphere.  The  connection  between  adjacent 
convolutions  and  lobes  is  established  by  means  of  the 
fibri^e  propricBy  while  more  remote  convolutions  and  lobes 
communicate  with  each  other  by  means  of  the  short  and 
long  association  bundles.  These  fibers  pass  from  convolu- 
tion to  convolution  within  the  hemisphere.  As  they  enter 
the  central  medullary  substance  they  are  collected  into 
larger  bundles,  which  again  subdivide  in  the  more  remote 
portions  of  the  cortex.  The  most  important  association 
bundles  are  : 

1.  The  cingulum,  placed  immediately  above  the  corpus 
callosum  and  uniting  the  gyrus  fornicatus  with  the  gyrus 
hippocampi  (association  paths  for  the  olfactory  nerve). 

2.  Fasciculus  uncinatus,  between  the  inferior  frontal 
convolution  and  the  temporal  lobe. 

3.  Fasciculus  longitudinalis  infeiior,  between  the  occipital 
and  temporal  lobes. 

4.  Fasciculus  longitudinalis  superior  (arcuatus),  connects 
the  frontal  lobe  with  the  parietal  and  also  with  the  tem- 
poral lobes. 

5.  Fasciculus  occipitqfrontalis  (tapetum),  connecting  the 

^  It  is  probable  that  the  corpus  callosum,  in  addition  to  the  com- 
missural fibers,  also  contains  association  filDers  connecting  the  two 
hemispheres.  Many  of  the  fibers  of  the  corpus  callosum  are  probably 
mere  collaterals  derived  from  the  long  bundles  of  association  fibers. 


ASSOCIATION  FIBERS. 


31 


frontal  lobe  with  the  occipital  and  temporal.  In  the 
frontal,  parietal,  and  occipital  lobes  the  association  bundles 
connecting  different  parts  of  the  same  lobe  and  the  other 


Fig.  7. 


Fig. 


Figs.  7  and  8. — The  long  association  fibers.  Figure  7  shows  the 
bundles  contained  in  the  lateral  white  substance  of  the  hemispheres  ; 
figure  8,  those  in  the  mesial  white  matter.  At  the  upper  border  a 
few  short  association  bundles  are  shown  diagrammatically. 


32  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

portions  of  the  cortex  on  the  same  side  are  especially 
numerous.  The  occipital  lobe  also  contains  the  fasciculus 
rectus  and  fasciculus  transversus. 

III.  The  Projection  Fibers. — These  are  the  most  im- 
portant fiber  tracts.  They  either  originate  or  end  in  every 
portion  of  the  cortex,  especially  in  the  convexity  of  the 
convolutions.  After  traversing  the  transverse  commissural 
and  longitudinal  association  fibers,  they  proceed  to  the 
deeper  portions  of  the  brain-stem  and  spinal  cord,  so  as  to 
establish  a  communication  between  them  and  the  cortex. 
The  term  corona  radiata  is  applied  to  the  entire  system  of 
projection  fibers.^ 

The  tracts  of  the  corona  radiata  are  divided  into  short 
and  long  fibers,  depending  on  the  point  at  which  their  axis- 
cylinders  subdivide  into  terminal  fibrils.  The  fibers  of 
the  corona  radiata  are  collected  into  a  compact  bundle  in 
the  internal  capsule  (anterior  and  posterior  limb),  and  in 
their  subsequent  course  downward  they  pass  through  the 
striate  body. 

1.  Short  Fibers  of  the  Corona  Radiata. — (a)  One  por- 
tion of  the  fibers  of  the  corona  radiata,  originating  in  all 
the  convolutions  of  the  cortex  and  being  contained  in  the 
internal  capsule,  enters  the  optic  thalamus  as  the  anterior, 
posterior,  and  inferior  peduncles  of  the  optic  thalamus  and 
is  lost  in  the  substance  of  that  structure  ;  others  spread 
out  over  the  surface  of  the  optic  thalamus  before  pene- 
trating its  substance  (stratum  zonale).  In  this  way  the 
optic  thalamus  receives  four  difi^erent  peduncles :  The 
anterior  peduncle,  from  the  frontal  lobe ;  the  superior 
peduncle,  from  the  frontal,  parietal,  and  temporal  lobes ; 
the  posterior  peduncle,  from  the  temporal  and  occipital 
lobes  ;  and  the  inferior  peduncle,  from  the  temporal  lobe. 

(b)  Another  tract  of  fibers  leaves  the  anterior  limb  of  the 

^  According  to  Flechsig,  projection  fibers  originate  only  in  the  cen- 
tral convolutions,  in  the  occipital  and  temporal  lobes,  while  in  the 
other  lobes  only  association  fibers  have  their  beginning. 


PROJECTION  FIBERS.  33 

« 
capsule  and  enters  the  caudate  nucleus.     (These  must  be 
regarded  as  association  fibers.) 

(c)  Finally,  a  bundle  of  fibers  derived  from  the  cuneus 
and  lingula  of  the  occipital  lobe  enters  the  posterior  segment 
of  the  posterior  limb  of  the  capsule,  and  thence  proceeds 
to  the  primary  optic  centers,  and  to  the  pulvinar,  lateral 
geniculate  body,  and  anterior  corpus  quadrigeminum. 
These  fibers  are  known  as  Gratiolet's  optic  radiation. 

2.  The  Long  Fibers  of  the  Corona  Rad'iata. — These  are 
also  derived  from  all  parts  of  the  cortex  ;  they  enter  the 
internal  capsule  and  proceed  downward  to  the  subthalamic 
region  underneath  the  optic  thalamus,  and  thence  either 
into  the  tegmental  or  into  the  ventral  portion  of  the  cere- 
bral peduncle. 

(o)  Tegmental  Fibers. — Their  exact  course  is  not  per- 
fectly known.  Some  of  them  enter  the  tegmentum  directly 
from  the  internal  capsule  (posterior  limb),  others  after 
traversing  the  inner  segments  of  the  lenticular  nucleus 
(lenticular  loop,  fillet  from  the  globus  pallidus)  and  break- 
ing through  that  portion  of  the  internal  capsule  which  lies 
to  the  mesial  side  of  these  structures.  The  fibers  either 
end  at  this  point  or  continue  downward  as  the  tract  of  the 
fillet  to  the  inferior  extremity  of  the  medulla  oblongata. 
From  recent  investigations  it  appears  probable  that  the 
fillet  is  interrupted  in  its  course  through  the  optic  thalamus. 
We  distinguish  ^  mesial  and  a  lateral  tract  of  the  fillet 
(central  sensory  pathway). 

{b)  Tracts  of  the  Crusta. — All  those  fibers  of  the  corona 
radiata  which  have  not  left  the  main  body  of  the  tract  now 
pass  from  the  internal  capsule  (anterior  and  posterior  limbs) 
into  the  crusta,  and  thus  leave  the  hemispheres  in  which 
they  originate. 

According  to  their  origin,  the  fibers  are  divided  into 
three  groups : 

a.  The  Mesial  Peduncular  Fibers. —  These  probably 
originate  in  the  cortex  of  the  frontal  lobe,  and,  after  tra- 


34 


MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 


versing  the  anterior  limb  of  the  capsule,  end  in  the  mesial 
ganglia  of  the  pons  (frontal  pontine  tract). 

ft.  The  Lateral  Peduncular  Fibers  (oval  bundle  — 
Tiirck's  bundle). — These  are  derived  from  the  temporal 
lobe.     They  pass  through  the  posterior  limb  of  the  capsule 


Fig.  9. — Section  through  the  frontal  lobe,  showing  the  beginning 
of  the  most  anterior  bundles  of  the  corona  radiata,  which  contain 
the  first  fibers  of  the  pyramidal  tract  {R):  c.  c.  Corpus  callosum;  C.  F, 
centrum  semiovale  Vieussenii;  c.  a,  anterior  limb  of  the  internal  cap- 
sule; /.  ?,  inferior  frontal  convolution  (base  of  the  third  frontal  con- 
volution— motor  speech  center).    For  the  other  letters  consult  Plate  28. 


and  end  in  the  collateral  ganglia  of  the  pons  (temporo- 
occipital  pontine  tract). 

y.   The  Middle  Peduncular  Fibers. 

The  Pyramidal  Tract. — These  fibers  originate  in  the 
cortical  cells  of  the  central  convolutions  and  their  imme- 


THE  PYRAMIDAL  TRACT. 


35 


diate  neighborhood,  and,  after  forming  part  of  the  corona 
radiata  (Fig.  9),  enter  the  internal  capsule,  where  they 
are  found  in  the  knee  and  in  the  anterior  third  of  the 
posterior  limb.  In  the  crusta  they  occupy  a  position  be- 
tween the  bundles  mentioned  under  a  and  i^.  (See  Plate  68.) 
This  portion  of  the  ventral  peduncular  fibers  emerges  at 
the  posterior  border  of  the  pons  in  a  compact  bundle, 
known  as  the  pyramid,  and  continues  its  way  down  the 
spinal  cord  as  tlie  pyramidal  tract.     Most  of  the  fibers, 


Fig.  10. — Schema  of  the  internal  capsule. 


as  has  already  been  stated,  undergo  decussation  and  occupy 
the  lateral  column,  while  the  smaller  uncrossed  portion 
remains  in  the  anterior  column.  This  tract  contains  the 
longest  fibers  of  the  corona  radiata,  and  can  be  followed  in 
the  lateral  column  of  either  side  as  far  down  as  the  conus 
medullaris.  From  the  cerebral  peduncle  onward  fibers  con- 
stantly leave  the  main  tract  and  pass  to  the  motor  nuclei 
of  the  opposite  side.  This  tract  forms  the  central  motor 
pathway. 


36  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

The  position  of  the  various  tracts  is  well  shown  in  the 
accompanying  schema  of  the  capsule  (Fig.  10),  modified 
from  Edinger. 

The  fibers  of  the  corona  radiata,  which,  as  we  have 
seen,  are  derived  from  the  cortex,  are  later  joined  by  other 
fibers  from  the  striate  body  and  optic  thalamus,  which 
continue  downward  as  short  tracts.     The  latter  include  : 

1.  The  fibers  running  from  the  caudate  nuclei  and 
putamen  to  the  optic  thalamus  (inner  segment  of  the  len- 
ticular nucleus)  and  further  downward  to  the  substantia 
nigra  in  the  crus  (basal  forebrain  bundle). 

2.  Fibers  beginning  in  the  optic  thalamus  and  ending 
in  the  tegmentum  and  corpus  albicans.  (See  Fig.  11.) 
These  contain  the  more  important  short  tracts  of  the  inter- 
bmin. 

The  following  fibers  take  their  origin  in  the  tegmentum: 
The  posterior  longitudinal  bundle,  situated  immedi- 
ately beneath  the  gray  matter  of  the  ventricle,  which  con- 
nects several  cranial  nerves  and  extends  as  far  down  as 
the  cervical  enlargement  (see  Fig.  11);  a  massive  bundle 
of  fibers  which  emerge  from  the  7'ed  nucleus  and,  after  decus- 
sating with  a  corresponding  bundle  from  the  opposite  side, 
form  the  superior  cerebellar  peduncle,  passing  as  such  to 
the  hemispheres  of  the  cerebellum  and  ending  in  the 
corpus  dentatum  and  cerebellar  cortex. 

In  the  cerebellum  the  following  fibers  are  found  : 
The  middle  cerebellar  peduncle,  which  passes  to  the 
pontine  ganglia  of  the  other  side,  where  its  fibers  end,  and 
the  inferior  cerebellar  peduncle,  going  to  the  medulla 
oblongata  (restiform  body).  These  bundles  contain  fibers 
connecting  the  cerebellum  with  the  olivary  bodies  and 
the  posterior  and  lateral  columns  (direct  cerebellar  tract) 
of  the  spinal  cord ;  some  of  these  form  long,  and  others 
short,  tracts. 

The  white  matter  of  the  cerebellum  also  contains  com= 
missural  and  association  fibers  similar  to  those  found  in 
the  cerebrum. 


SHORT  TRACTS  IN  BRAIN-STEM  AND  INTERBRAIN.     37 


For  the  manner  in  which  the  white  matter  of  the  spinal 
cord  is  constructed  from  the  projection  fibers  of  the  cere- 


Fig.  11. — The  short  tracts  in  the  brain-stem  and  interbrain.  Sagit- 
tal section  through  the  middle  of  the  brain-stem:  in/,  Infuudibulum; 
c.  mam,  corpus  mammillare;  fasc.  Vic,  bundles  of  Vicq  d'Azyr;  /.  teg, 
tegmental  bundle;  ^ed.  m,  peduncle  of  corpus  mammillare ;/asc.  rt,  fas- 
ciculus retroflexus;  fasc.  I.  inf,  posterior  longitudinal  bundle;  II,  III, 
VI,  XII,  corresponding  cranial  nerves;  c,  pineal  gland. 

bral  and  cerebellar  cortex,  the  pyramids,  restiform  bodies, 
etc.,  consult  a  former  paragraph  (p.  15). 


38  MORPHOLOGY  OF  THE  NERVOUS  SYSTEM. 

In  a  section  of  the  spinal  cord  we  see  the  two  halves 
separated  in  front  by  the  anterior  longitudinal  fissure. 
Immediately  behind  this,  in  the  median  line,  is  the  white 
anterior  commissure,  connecting  one  anterior  column  or, 
rather,  anterior  horn,  with  that  of  the  other  side.  Yen- 
trally  from  this  is  the  central  canal,  which  is  for  the  most 
part  obliterated,  and  behind  the  latter,  the  narrow  poste- 
rior commissure. 

The  gray  matter  forms  the  anterior  and  posterior  horns, 
and  is  surrounded  by  the  anterior,  lateral,  and  posterior 
columns  of  the  cord. 

1.  The  anterior  column  contains  the  uncrossed  pyr- 
amidal tract  and  the  anterior  ground  bundle  (continuations 
of  the  constituent  parts  of  the  substantia  reticularis  in  the 
tegmentum). 

2.  The  lateral  column  contains  the  crossed  pyramidal 
tract,  the  direct  cerebellar  tract  (from  the  restiform  body), 
the  tract  of  Gowers  (from  the  vermiform  process  of  the 
cerebellum),  the  anterolateral  ground  bundle,  and  the 
mixed  lateral  zone  (partly  derived  from  the  tegmentum). 

3.  The  posterior  column  contains  the  columns  of  GoU 
and  Burdach  and  the  root-zones. 

In  addition  to  the  fibers  derived  from  the  brain  the 
spinal  cord  contains  numerous  fibers  originating  within  its 
own  substance  (myelogenic,  intramedullary  fibers),  and  also 
fibers  which  come  from  the  periphery  (extraspinal  fibers). 

A  more  detailed  description  of  the  course  and  signifi- 
cance of  the  pathways  that  have  been  mentioned  and  of 
others  will  be  found  in  Part  III.  The  foregoing,  it  is 
hoped,  will  serve  to  explain  tlie  serial  sections  contained 
in  Plates  28  to  52,  which  are  intended  as  an  introduction 
to  the  study  of  the  topogra})hic  anatomy  of  the  brain. 
The  more  complex  relations  between  the  gray  matter  of 
the  cortex,  basal  ganglia,  optic  thalamus,  and  nuclei  of  the 
cranial  nerves  can  only  be  studied  from  the  illustrations, 
and  the  reader  is  therefore  referred  to  the  plates  and  to 
the  explanatory  notes  which  accompany  them. 


PART   III. 

ANATOMY  AND  PHYSIOLOGY  OF  THE 
MORE  IMPORTANT  NERVOUS  PATH- 
WAYS^ 

(Plates  54  to  57.) 


We  understand  by  nervous  pathway  the  anatomic  basis 
for  the  transmission  of  a  definite  physiologic  impulse  from 
the  ganglion  cell  to  the  end-organ  which  receives  the  im- 
pulse, including  all  the  connections. 

Every  physiologic  function  requires  for  its  completion 
a  nervous  jmthway  which  is  composed  of  a  number  of 
communicating  neuron  complexes,  each  individual  neuron 
complex  completely  retaining  its  physiologic  and  anatomic 
independence.  Thus  there  are  pathways  which  consist  of 
two,  three,  or  even  more  successive  neuron  complexes. 
The  more  important  of  these  belong  to  the  projection 
system  of  the  cerebral  and  cerebellar  cortex.  They  are  the 
following  : 

Nerve  Tracts  Associated  with  Known  Functions. 

1.  The  motor,  corticomuscular,  or  centrifugal  tract,  con- 
sisting of  two  neuron  complexes. 

2.  The  sensory,  centripetal  tract,  consisting  of  at  least 
three,  and  probably  more,  neuron  complexes. 

Tliese  two  tracts  communicate  with  each  other  in  two 
different  divisions  of  their  course  : 

(a)  They  have  a  lower  connection,  which  forms  the  re- 
flex tract  and  is  not  under  the  influence  of  the  will.     It  is 

39 


40  THE  NEB  VO  US  FA  THWA  VS. 

found  in  the  subcortical  nuclei  (the  basal  ganglia ;  nuclei 
of  pons,  medulla,  and  cord). 

(6)  An  upper  connection  in  the  cortex,  the  pathway  of 
the  reactions  of  conscious  volition. 

The  course  of  the  motor  tract  is  much  better  known  and 
much  simpler  than  that  of  the  sensory  tract.  We  shall 
now  proceed  to  consider  these  tracts  and  their  communi- 
cations, in  the  order  named. 

1.  The  Motor  Pathway. 

The  pathway  considered  as  a  whole  is  composed  of 
two  successive  neuron  complexes,  the  central,  or  archi- 
neuron,  and  the  peiipheral  motor,  or  teleneuron.  The  cells 
of  the  central  neurons,  situated  in  the  central  convolutions 
of  the  cerebral  cortex, — pyramidal  cells  of  the  cortex, — 
send  their  nerve-fibers  in  a  compact  body,  known  as  the 
pyramidal  tract,  by  way  of  the  corona  radiata,  through  the 
knee  and  anterior  third  of  the  posterior  limb  of  the  internal 
capsule  into  the  crusta.  From  there  they  are  continued 
by  way  of  the  pons  into  the  pyramids. 

At  the  decussation  of  the  pyramids  the  greater  part  of 
the  fibers  enter  the  lateral  column  of  the  cord,  which  is 
continued  as  the  crossed  lateral  pyramidal  tract.  In  the 
cervical  enlargement  these  fibers  are  situated  in  the  median 
portion  of  the  lateral  column,  and  as  they  proceed  down- 
ward approach  nearer  and  nearer  to  the  periphery  of  the 
cord,  terminating  finally  in  the  conns  medullaris.  A 
smaller  number  of  the  nerve-fibers  are  continued  without 
decussation  in  the  anterior  pyramidal  tract,  and  do  not 
extend  lower  than  the  upper  portion  of  the  lumbar  en- 
largement. 

Along  the  entire  extent  of  this  tract,  beginning  at  the 
crusta,  certain  nerve  bundles  leave  the  tract  at  various 
levels  and,  after  undergoing  decussation,  pass  to  the  other 
side.  (See  Fig.  14,  which  represents  an  anterior  view  of 
the  pyramidal  tract.)      These  nerve-fibers  split  up  into 


THE  MOTOR  PATHWAY. 


41 


terminal  fibrils  which  end  in  the  motor  nuclei  of  the  brain 
and  spinal  marrow.  It  follows,  therefore,  that  the  entire 
mass  of  fibers  contained  in  the  pyramidal  tract  gradually 
diminishes  from  above  downward.  In  addition  other  col- 
lateral fibers  are  given  off  from  the  decussating  fibers  and 


N  ivQior 


Fig.  12. —Schema  of 
the  motor  pathway :  c, 
Central,  ^,  peripheral,  neu- 
ron; d^  decussation;  Jf, 
muscle. 


Fig.  13. — Schema  showing  the  course 
of  the  pyramidal  tract:  /,  In  the  cere- 
brum and  crus;  //,  in  the  pons;  ///,  in 
the  medulla  oblongata;  /F,  decussation 
of  the  pyramids —  F,  in  the  cervical  en- 
largement; F/,  in  the  lumbar  enlarge- 
ment. 


pass  to  higher  nuclei.  Thus  the  entire  central  mass  of 
neurons  finally  splits  up  in  the  substations  which  have 
been  described  as  situated  at  various  levels  of  the  brain 
and  spinal  marrow.     (See  Fig.  13.) 

These  terminal  nerve  fibrils  surround  the  dendrons  of 


42 


THE  NERVOUS  PATHWAYS. 


the  ganglion  cells  of  the  peripheral  motor  neurons  which 
begin  at  this  point — I.  e,,  at  the  substation  just  men- 
tioned. 

The  nerve  processes  of  these  cells  emerge  as  nerve- 
roots  from  the  brain  and  anterior  horn  of  the  spinal  cord 
of  the  same  side,  and  are  continued  as  motor  fibers  to  the 
muscle,  where  they  finally  break  up  into  their  terminal 
fibrils  among  the  individual  muscle-fibers.     The  central 

motor  neuron,  therefore,  un- 
dergoes decussation,  while 
the  peripheral  does  not. 
(See  Fig.  12.)  The  im- 
pulses which  originate  in 
the  cells  of  the  cortex  are 
transmitted  to  the  muscle 
through  the  pathway  formed 
of  these  two  neurons,  and 
from  the  decussation  of  the 
central  neurons  it  follows 
that  the  cortex  of  each  hemi- 
spliere  controls  the  muscles 
of  the  opposite  half  of  the 
body. 

Every  neuron  cell  exer- 
cises a  trophic  influence  on 
its  processes,  including  the 
long  axis-cylinder  process. 
If  this  influence  is  de- 
stroyed, the  corresponding 
nerve -fiber  undergoes  de- 
generation, and  the  gan- 
glion cell  itself  suffers  degenerative  changes  if  the  con- 
tinuity of  the  neuron  is  interrupted.  The  cell  of  the  per- 
ipheral neuron  in  addition  exercises  a  nutritive  influence 
on  the  muscle-fibers  to  which  it  is  distributed. 

The  most  important  constituents  of  the  motor  pathway, 
taken  in  the  order  in  which  the  peripheral  nerve  tracts 


4A     Jh^ 

^^^Hi^/w/^' 

^~^^^^Wf 

^^^r\:\ 

/w'%  |l>„  y  \ 

w>s-|||^  v^ 

V  ll  JL-', 

■  -Decu&suUo 
pynvmidum'. 

w^ 

Fig.  14. — Schema  showing  the 
I)osition  of  the  pyramidal  tnict 
{Py)  in  the  mesencephalon:  ///, 
F,  Vll,  XII,  Central  motor  path- 
ways to  the  corresponding  cranial 
nerves. 


THE  MOTOR  PATHWAY.  43 

emerge  from  the  brain  from  above  downward,  are  the  fol- 
lowing : 

1.  Oculomotor  Nerve. — The  central  neuron  complex 
originates  at  some  unknown  point  in  the  cortex  (angular 
gyrus?),  passes  through  the  knee  of  the  internal  capsule, 
and  leaves  the  pyramidal  tract  in  the  peduncle  of  the  cere- 


Fig.  15. — Oculomotor  nucleus  (medullary  sheath  stain;  photo- 
graph, magnified  150  times):  jP,  Fasc.  long,  post.;  A.S^  aqueduct 
of  Sylvius;  d,  dorsal,  v,  ventral,  c,  central,  nucleus.  Note  the  decussa- 
tion of  the  root-fibers  from  the  ventral  nucleus. 


brum,  perhaps  forming  a  part  of  Spitzka's  bundle  or  acces- 
sory fillet.  (See  Plate  42.)  The  latter  arises  from  the 
mesial  portion  of  the  pyramidal  region  in  the  peduncle, 
and,  after  turning  inward  and  upward  and  crossing  the 
middle  line,  ends  in  the  oculomotor  nucleus  of  the  oppo- 
site (and  of  the  same  ?)  side,  which  is  situated  in  the  cen- 


44  THE  NEB  VO US  FA THWA  VS. 

tral  gray  matter,  underneath  the  aqueduct  of  Sylvius. 
The  terminal  fibers  of  the  central  neuron  of  the  oculo- 
motor surround  the  ganglion  cells  that  are  found  in  this 
region.  These  cells  and  their  dendrites  form  the  first  por- 
tion of  the  peripheral  neuron.  The  nerve-fibers  emerge 
from  the  nucleus  as  the  roots  of  the  oculomotor  nerve  on 
the  same  and,  to  some  extent,  on  the  opposite  side,  and  are 
continued  in  the  trunk  of  the  oculomotor  nerve  to  the  ocular 
muscles.  (For  a  further  description  of  their  distribution 
and  function  see  explanation  to  Plate  37.)  The  position 
and  divisions  of  the  oculomotor  nucleus  are  seen  in  the 
accompanying  Figure  15  ;  see  also  Figure  29,  on  p.  184, 
and  Figure  17.  The  latter  also  shows  the  probable  rela- 
tion of  the  divisions  of  the  nucleus  to  the  individual 
muscles. 

2.  Trochlear  Nerve. — The  course  of  the  central  neuron 
is  the  same  as  that  of  the  oculomotor.  After  undergoing 
decussation  the  end-fibers  break  up  in  the  trochlear  nucleus 
of  the  opposite  side,  under  the  posterior  corpora  quadri- 
gemina  and  behind  the  oculomotor  nucleus.  The  periph- 
eral neuron  begins  at  this  point,  emerging  as  the  trochlear 
nerve  behind  the  quadrigemina,  and  crossing  with  all  its 
fibers  the  nerve  of  the  opposite  side  in  the  anterior  medul- 
lary velum. 

3.  Motor  Portion  of  the  Fifth  Nerve. — The  central 
neuron  originates  at  some  unknown  point  in  the  cortex 
(inferior  parietal  gyrus?),  traverses  the  knee  of  the  in- 
ternal capsule  behind  the  fibers  of  the  oculomotor,  and 
leaves  the  peduncle  in  Spitzka's  bundle  (?).  It  undergoes 
decussation  in  the  raphe  of  the  tegmentum  (accessory 
fillet),  and  surrounds  with  its  end-fibers  the  cells  of  the 
motor  nucleus  of  the  fifth  nerve,  which  is  situated  in  the 
lateral  portion  of  the  tegmentum.  From  this  point  the 
peripheral  neuron  is  continued  as  the  motor  root  of  the 
fifth  nerve,  emerging  from  the  pons  as  the  anterior  root, 
after  receiving  some  fibers  from  the  motor  nucleus  of  the 
opposite  side.     The  nasal  root  of  the  fifth  nerve  (formerly 


THE  MOTOR  PATHWAY.  45 

known  as  the  ascending  root)  is  also  said  to  contain  motor 
(trophic  ?)  fibers.  It  originates  in  the  lateral  portion  of 
the  central  gray  matter  of  the  aqneduct  of  Sylvius,  from 
the  large  cells  which  are  situated  in  the  lower  part  of  that 
region,  and  joins  the  anterior  root  of  the  fifth  nerve  at  its 
exit  from  the  brain. 

4.  Abducens. — Tlie  course  of  the  central  neuron  is  tlie 
same  as  for  the  oculomotor.  After  undergoing  decussation 
the  end-fibers  split  up  in  the  abducens  nucleus,  underneath 
the  floor  of  the  fourth  ventricle,  near  the  median  line. 
The  peripheral  neuron  is  given  off  from  the  cells  of  the 
abducens  nucleus,  and,  after  traversing  the  posterior  por- 
tion of  the  pons,  emerges  as  the  abducens  nerve. 

5.  Facial  Nerve. — The  central  neuron  complex  origi- 
nates in  the  cells  of  the  lower  third  of  the  central  convolu- 
tions. From  here  the  tract  proceeds  in  the  posterior  limb 
of  the  internal  capsule,  behind  the  knee,  separates  from 
the  pyramidal  tract  in  Spitzka's  bundle,  and,  after  decus- 
sating in  the  raphe  of  the  tegmentum,  joins  the  long  facial 
nucleus  of  the  opposite  side,  wliich  is  situated  in  the  deeper 
portions  of  the  medulla  oblongata,  laterally  from  the  teg- 
mentum. From  this  point  the  individual  fibers  of  the 
facial  nerve,  forming  the  peripheral  neuron,  pass  upward 
and  inward  to  the  genu  of  the  facial,  and  arch  outward 
and  then  downward  until  they  finally  emerge  from  the 
medulla  oblongata  as  the  facial  nerve.  This  is  the  "  lower  " 
facial  nerve  (mouth  and^  cheeks). 

The  central  neuron  for  the  "  upper  "  facial  nerve  (brow) 
apparently  follows  some  other  course  which  is  not  known. 
The  peripheral  neuron  is  said  to  emerge  from  the  posterior 
segment  of  the  oculomotor  nucleus  and  finally  to  reach  the 
trunk  of  the  facial. 

The  branch  which  supplies  the  orbicularis  oris  is  said 
to  contain  fibers  from  the  nucleus  of  the  hypoglossus  (?) 

6.  Motor  Portion  of  the  Glossopharyngeovagus. — 
The  central  neuron  originates  in  some  unknown  portion  of 
the  cortex  (middle  frontal  convolution  ?),  descends  in  the 


46  THE  NEB  VO  US  PA  THWA  VS. 

pyramidal  tract,  and,  after  crossing  in  the  raphe,  reaches 
in  some  unknown  way  the  nucleus  ambiguus,  which  is  as- 
sumed to  be  its  motor  nucleus.  The  latter  is  found  in  the 
prolongation  of  the  facial  nucleus  within  the  posterior 
portion  of  the  medulla  oblongata.  From  this  point  the 
fibers  of  the  peripheral  neuron  for  the  most  part  join  the 
vagus. 


Fig.  16. — Nticlens  of  the  right  hypoglossus  fstained  with  methylene- 
blne;  photograph,  magnified  150  times):  V,  Rhomboid  fossa;  iy,  post, 
long,  bundle;  E,  raphe;  IX,  glossopharyngeo vagus  nucleus;  S, 
Roller's  accessory  nucleus. 


7.  Hypoglossus. — The  central  neuron  originates  in  the 
lower  third  of  the  central  convolutions  in  front  of  the 
facial  center,  descends  in  the  internal  capsule  behind  the 
path  of  the  facial,  leaving  the  pyramidal  tract  in  the  ac- 
cessory fillet.     After  crossing  in  the   raphe  of  the  teg- 


THE  310 TOE  PATHWAY.  47 

mentum  it  enters  the  hypoglossus  nucleus  of  the  opposite 
side,  among  the  cells  of  which  it  finally  breaks  up.  (See 
Fig.  16.)  At  this  point  the  peripheral  neuron  emerges 
from  the  medulla  as  the  hypoglossus  nerv^e. 

The  nerve  paths  described  in  5,  6,  and  7 — that  is,  those 
which  originate  in  tlie  left  hemisphere — ^are  especially  con- 
cerned in  the  act  of  speech.  Their  central  neurons  to- 
gether form  the  central  speech  path,  while  their  peripheral 
neurons  form  the  peripheral  speech  path.  The  existence  of 
a  separate  speech  path  has  also  been  assumed  but  has  never 
been  proved. 

8.  Spinal  Accessory  Nerve. — The  central  neuron  is 
said  to  originate  in  the  base  of  the  middle  frontal  con- 
volution (?)  and  to  follow  the  pyramidal  tract.  Its  sub- 
sequent course  is  unknown,  but  it  eventually  enters  the 
accessory  nucleus  of  the  opposite  side,  in  the  lower  portion 
of  the  medulla  and  upper  portion  of  the  cervical  enlarge- 
ment. From  this  point  the  peripheral  neuron  proceeds  as 
the  spinal  accessory  nerve.  A  large  part  of  the  nerve — 
the  internal  branch — joins  the  pneumogastric. 

9.  The  Motor  Pathway  of  the  Upper  Extremity. — 
The  central  neuron  complex  originates  in  the  cells  of  the 
middle  third  of  the  central  convolutions,  especially  of  the 
anterior  convolution,  passes  down  through  the  posterior 
limb  of  the  internal  capsule  in  its  anterior  third,  and  enters 
the  pyramidal  tract,  which  it  accompanies  through  the 
ventral  portion  of  the  peduncle  and  pons  into  the  pyramid. 
At  the  decussation  of  the  pyramids  the  greater  part  passes 
to  the  lateral  column  of  the  opposite  side,  while  a  smaller 
portion  descends,  without  decussating,  in  the  anterior 
column  of  the  cord  (individual  variations  occur  in  this 
respect).  At  the  level  of  the  cervical  enlargement  the 
fibers  are  successively  reflected  at  a  right  angle,  and  pass 
— those  from  the  lateral  pyramidal  tract  into  the  anterior 
horn  of  the  same  side,  and  those  from  the  anterior  pyr- 
amidal tract  by  way  of  the  anterior  commissure  into  the 


48  THE  NERVOUS  PATHWA YS. 

anterior  horn  of  the  opposite  side.  ^  Here  the  terminal 
fibers  surround  the  cells  of  tlie  anterior  horn  (especially 
the  lateral  groups)  and  their  dendrons. 

These  cells  form  the  beginning  of  the  peripheral  neuron 
of  the  motor  tract.  The  nerve  processes  emerge  as  the 
anterior  roots  (fourth  cervical  to  first  dorsal),  and  reach 
the  brachial  plexus,  from  which  they  are  continued  into 
the  various  nerves  of  the  arm.  (For  detailed  description 
see  the  explanation  of  Plate  27.)  The  situation  of  the 
cells  of  the  anterior  horn  and  their  relation  to  the  indi- 
vidual muscles  are  best  seen  in  Figure  17  on  page  52. 

The  nerve  tracts  for  the  upper  extremity  are  situated 
between  those  which  supply  the  muscles  of  the  neck  above, 
and  those  which  supply  the  muscles  of  the  trunk  below. 
The  topography  can  readily  be  understood  by  a  study  of 
the  plates  mentioned ;  but  little  is  known  concerning  the 
central  course  of  the  tract.  The  center  for  movements  of 
the  trunk  is  said  to  be  situated  in  the  superior  frontal  con- 
volutions. It  is  probable  that  the  pathway  originates  in 
the  hemispheres  both  of  the  same  and  of  the  opposite  side. 
In  the  same  way  other  muscles  whose  functions  are  bilat- 
eral (eye,  brow  muscles,  etc.)  probably  derive  their  inner- 
vation from  the  hemispheres  both  of  the  same  and  of  the 
opposite  side.  But  our  knowledge  of  these  uncrossed  (or 
double  crossed  ?)  central  pathways  in  man  is  very  imper- 
fect (uncrossed  anterior  pyramid  ?).     (See  foot-note.) 

10.  The  Motor  Pathway  for  the  Lov^^er  Extremity. — 
The  central  neuron  originates  in  the  upper  third  of  the  cen- 
tral convolutions  and  in  the  paracentral  lobule.  It  is  con- 
tinued in  the  pyramidal  tract  through  the  posterior  limb 
of  the  internal  capsule  (in  the  center  of  the  limb),  and 
proceeds  downward  as  described  under  9 — ^that  is  to  say, 
it  undergoes  a  partial  decussation  at  a  lower  level  than 
that  of  the  upper  extremity.    The  great  mass  of  the  fibers 

^  This  ultimate  decussation  of  the  anterior  pyramidal  tract  has 
recently  been  disputed,  with  some  reason,  and  it  has  been  supposed 
that  the  tract  ends  in  the  anterior  horn  of  the  same  side. 


THE  SENSOR  Y  PA  THWA  Y.  49 

descend  in  the  lateral  pyramidal  tract  as  far  as  the  lum- 
bar enlargement,  where  they  are  reflected  into  the  ante- 
rior horn  and  break  up  into  their  terminal  fibrils. 
From  the  cells  of  the  anterior  horn,  especially  those  of 
the  lateral  groups,  the  peripheral  neuron  emerges  as  the 
anterior  roots  (five  lumbar  and  five  sacral),  enters  the 
lumbar  and  sacral  plexuses,  and  is  continued  from  these 
plexuses  into  the  nerves  of  the  lower  extremities.  (See 
Plate  27  and  Fig.  17,  in  which  the  relations  of  the 
muscles  to  the  various  divisions  of  the  peduncle  and 
of  the  spinal  cord  on  the  right  side  of  the  body  are 
shown.) 

11.  The  motor  pathway  for  the  bladder,  rectum,  and 
sexual  organs  arises  at  some  unknown  point  in  the  brain, 
the  central  neuron  descending  in  the  pyramidal  lateral 
tract,  probably  in  the  anterolateral  ground  bundle,  and 
terminating  in  the  gray  matter  of  the  sacral  cord.  The 
pei'ipheral  neuron  emerges  as  the  second,  third,  and  fourth 
sacral  roots,  and  goes  to  the  pudendal  plexuses  and  finally 
to  the  muscles  of  the  organs  named.     (See  Plate  27.) 

12.  The  sympathetic  nerve  receives  central  motor 
fibers  of  unknown  cortical  origin  from  the  lateral  col- 
umns. They  appear  to  end  in  the  anterior,  and  especially 
in  the  lateral,  horn.  At  this  point  the  peripheral  neuron 
begins;  it  emerges  in  the  anterior  roots,  and  is  finally  dis- 
tributed to  the  ganglions  of  the  sympathetic  nerves  and 
their  homologues.  The  cells  in  these  ganglia  form  the 
beginning  of  the  motor  sympathetic  neuron,  the  fibers  of 
which  are  distributed  to  the  various  unstriped  muscle- 
fibers  in  the  vessels,  intestines,  heart  (?),  glands,  etc.  The 
vasomotor  nerves  also  have  their  origin  in  the  antero- 
lateral ground  bundle. 

II.  The  Sensory  Pathway. 

Since  the  function  of  the  sensory  pathway  is  to  transmit 
sensory  impressions  from  the  periphery  to  the  center,  we 
4 


50  THE  NEB  VO  US  PA  THWA  YS. 

shall  describe   it  in  this  direction,  beginning,  therefore, 
with  the  peripheral  neuron. 

The  peripheral  sensory  neuron  complex  of  the  ex- 
tremities and  of  the  trunlv  is  contained  in  the  sensory 
fibers  of  the  peripheral  nerves,  the  cutaneous  distribu- 
tion of  which  is  seen  in  Figures  23  to  25  and  in 
Figure  17.  It  continues  its  course  to  tlie  spine  through 
the  fibers  of  the  various  plexuses,  and  ends  in  the  cells  of 
the  spinal  ganglia  (without  directly  entering  the  spinal 
cord).  Each  cell  of  the  spinal  ganglia  gives  off  another 
fiber  in  the  opposite  direction.  These  fibers  collectively 
form  the  posterior  roots,  and  as  such  the  sensory  periph- 
eral neuron  finally  reaches  the  spinal  marrow,  the  posterior 
roots  entering  in  two  separate  parts  into  the  posterior  col- 
umns that  lie  between  the  posterior  horns.  After  its 
entrance  into  the  spinal  cord  each  root-fiber  divides  in  the 
form  of  a  T,  and  gives  off  an  ascending  and  a  descending 
branch.     The  two  divisions  of  the  posterior  roots  are  : 

1.  The  lesser,  lateral  division  of  the  posterior  root,  which 
enters  the  tip  of  the  posterior  horn  in  the  region  known 
as  Lissauer's  tract,  where  each  of  its  fibers  divides  into  an 
ascending  and  a  descending  branch.  The  course  of  both 
branches  is  very  short :  after  running  a  short  distance 
within  the  cord,  they  are  reflected  at  right  angles  into  the 
posterior  horn  and  there  undergo  division  into  their  ter- 
minal fibrils  around  the  cells  of  the  posterior  horn. 

2.  The  larger y  mesial  division  of  the  posterior  root,  which 
enters  the  lateral  portion  of  the  posterior  column  (Bur- 
dach's  column),  and  is,  therefore,  known  as  the  posterior 
root-zone.  Here  the  fibers  split  up  into  an  ascending 
and  a  descending  branch. 

The  descending  branches  extend  but  a  short  distance, 
and  are  soon  reflected  at  right  angles  into  the  posterior 
horn,  where  they  undergo  arborization  ;  some  of  the  ascend- 
ing branches  are  also  short ;  others  have  a  longer  course. 

The  short  branches  are  soon  reflected  and  pass  partly 
into  the  posterior  horn,  partly  into  the  anterior  horn,  and 


THE  SENSOR Y  PA  THWA  Y.  51 

into  the  columns  of  Clarke,  where  they  break  up  among 
the  cells.  The  long  fibers  first  continue  their  way  in 
Burdach's  column  toward  the  brain,  but  as  tliey  are  joined 
by  other  ascending  root-fibers  at  higher  levels  they  grad- 
ually approach  nearer  to  the  median  line.  The  long  fibers 
that  enter  the  lumbar  enlargement  are,  therefore,  found  in 
the  column  of  GoU  in  the  cervical  region,  while  those  that 
enter  at  a  higher  level,  in  the  thoracic  and  cervical  portion 
of  the  cord,  occupy  a  more  external  position. 

These  long  ascending  fibers  eventually  break  up  into 
their  terminal  fibrils  within  the  medulla  oblongata,  about 
the  cells  of  the  nucleus  funiculus  of  Goll  (f.  gracilis) 
and  the  nucleus  funiculus  of  Burdach  (f  cuneatus). 

All  these  fibers  taken  together  form  the  i<ensory  periphey^al 
neuron  complex.  The  cell  of  this  neuron  is,  therefore,  situ- 
ated outside  of  the  spinal  cord,  in  the  intervertebral  ganglia  ; 
its  dendritic  processes  are  represented  by  the  peripheral 
nerve  and  its  principal  cutaneous  branches,  while  the  nerve 
process  corresponds  to  the  posterior  root-fiber  and  its  ter- 
minal fibrils  in  the  various  portions  and  levels  of  the  spinal 
cord. 

These  terminal  divisions  take  place  about  the  nerve- 
cells  lyiug  in  the  following  regions : 

1.  In  GolPs  and  Burdach's  nuclei  (funiculus  gracilis 
and  funiculus  cuneatus)  in  the  medulla  oblongata. 

2.  In  the  various  portions  of  the  posterior  horns. 

3.  In  the  so-called  middle  zones,  between  the  anterior 
and  the  posterior  horn. 

4.  In  the  columns  of  Clarke. 

5.  In  the  anterior  horn. 

The  central  sensory  neuron  complex  begins  in  the 
regions  included  under  1  to  4.  (For  the  nerve  termina- 
tions under  5  see  Reflex  Paths.)  Up  to  this  point  the  dis- 
tribution is  fairly  well  settled,  but  the  further  course  of  the 
central  sensory  tract  is  still  a  matter  of  dispute,  although 
it  is  very  much  better  understood  now  than  formerly. 
The  points  still  under  discussion  will  be  referred  to  briefly 


LOCATION  OF  THE  SEGMENTS  FOR 
Sensibility.  Motility. 


Supply  of 


Thoracic  and  abdominal 
viscera 
Occipital  region 

Front  of  neck 
Back  o, 

Shoulder 
Musculo 
spiral 
Median  n, 


Inferior  abdominal  reflex 

Gluteal  region 

Inguinal  region 

Hips 

Anterior 

Median 

External 

Posterior 

Internal 

External 

Foot 

Scrotum,  penis,  etc. 

Bladder,  rectum 

Anus 


Thigh 


II 


Sphincter  iridis 
Ciliaria 
„^  Rectus  int.,  levator  palpebr.  sup. 
Rectus  inf.  and  sup. 
Obi.  infer. 

Obi.  super. 

Masseter,  temporal,  pterygoids 

Rectus  extern. 

Occipitofront.,  orbicularis  octUi  (upper  facial) 
Muscles  of  expression  (lower  facial) 
^  Palatal  and  pharyngeal  muscles 
—  Muscles  of  the  larynx 
—  Muscles  of  the  tongue 

Sternocleidomastoid 
Deep  muscles  of  the  neck 
Scaleni 

Trapezius,  serratus  anticus 

Diaphragm 

Delt.,  biceps,  pectoral,  maj.  (clavic.  portion) 

Brachial,  antic,  supinator  longus 

Tricpps,  latis.  dorsi,  pect.  maj.  (costal     ' '     ) 

Extensores  carpi  et  digitorum  -> 

Flexor es  carpi  et  digitorum     ]  forearm 

Interossei,  lumbricales  ^ 

Thenar,  hypothenar     ) 

Intercostals 
Muscles  of  the  back 
Abdominal  muscles 


~—  Iliopsoas    \ 
-~—  Sartorius    | 

Adductors  \  ^'"'9" 

— -  Abductors  J 
""'  Quadriceps  f 

.Flexors        (Leg 

"'..-  Extensors    } 
Peronei 

i-'lexors,  extensors  of  the  foot  and  toes 
'Glutei  (?) 
Perineal ', 

Vesical    >  Musculature 

Rectal 


Fig.  17. — Explanation  of  abbreviations:  tr.  oJf,  Olfactory  tract; 
c.  g.  7,  lateral  geniculate  body;  p,  r,  cr,  A,  indicate  approximately  tlie 
location  of  the  reflex  centers  for  the  pupillary  (j»),  the  respiratoiy 
(r),  cremasteric  (cr),  patellar  {pat),  and  tendo  Achillis  {A)  reflexes, 

52 


THE  SENSOR  Y  PA  TH  WA  Y. 


53 


in  a  subsequent  paragraph ;  what  follows  is  that  descrip- 
tion of  the   subsequent  course  of  the  neuron  which  har- 
monizes   best    with    the   postulates   of    pathology.      The 
anatomic  distribution  in  man  is  not 
absolutely  known. 

The  beginning  of  the  central  sen- 
sory neuron,  corresponding  with  the 
terminal  divisions  of  the  peripheral 
neuron,  is  found  partly  in  the  above- 
mentioned  regions  of  the  medulla 
oblongata,  and  partly  in  the  gray 
matter  of  the  posterior  and  anterior 
horns  of  the  cord.  We  w^ill  discuss 
the  separate  portions  in  the  order  in 
which  they  are  given  above — 1  to  4. 

1.  The  central  neuron  has  its  or- 
igin in  the  cells  of  the  funiculus 
gracilis  and  funiculus  cuneatus  in 
the  medulla  oblongata.  From  this 
point  the  fibers  pass  downward  and 
toward  the  raphe,  forming  the  inter- 
nal arcuate  fibers  ;  at  this  point  they 
cross  the  median  line  (decussation 
of  the  fillet,  the  beginning  is  seen 
in  Plate  46,  Fig.  1  (fai) ;  it  ends 
at  the  level  shown  in  Plate  44,  Fig. 
2).     Above    this    decussation    the 

fibers,  after  being  collected  into  a  bundle,  pass  dorsally 
and  above  the    pyramids   (which  have  decussated  at   a 


Fig.  18.  —  Schema 
of  the  sensory  pathway: 
c,  Central,  p,  peripheral, 
neuron ;  g^  interverte- 
bral ganglion  cell;  b, 
short,  I,  long,  tract;  d, 
decussation. 


The  vesical  center  lies  in  the  third  and  fourth  sacral  segments;  the  anal 
center  in  the  fourth  and  fifth '  represented  by  circles) ;  the  centers  for  erec- 
tion, ejaculation,  labor  pains  (?)  are  probably  also  situated  in  this  region. 
In  reality  the  divisions  between  the  various  segments  are,  of 
course,  not  so  sharp  as  they  are  shown  in  the  diagram,  so  that  a  given 
muscle  or  cutaneous  region  derives  some  of  its  controlling  nerve-roots 
from  the  segments  lying  immediately  above  and  below  the  principal 
segment.  The  sensory  segment  for  any  given  region  is  regularly  some- 
what higher  than  the  corresponding  motor  segment. 


54 


THE  NERVOUS  PATHWAYS. 


lower  point),  and  lie  next  to  the  anterior  ground  bundle, 
where  they  are  known  as  the  fillet  (laqueus  superior).  In 
its  subsequent  brainward  course  the 
fillet  gradually  increases  in  size  and 
ranges  itself  between  the  superior 
and  inferior  olives  that  now  make 
their  appearance,  forming  the  in- 
terolivary  layer,  still  close  to  the 
median  line.  Higher  up  the  fillet 
proceeds  in  the  region  of  the  teg- 
mentum, where  it  broadens  out  and 
lies  transversely  beneath  the  teg- 
mentum, being  known  at  this  point 
as  the  median  fillet.  In  this  way 
it  passes  through  the  dorsal  por- 
tion of  the  pons.  In  the  tegmen- 
tum it  leaves  the  median  line  and 
assumes  a  position  to  the  outer 
side  of  the  red  nucleus.  From 
this  point  the  superior  fillet  is  con- 
tinued to  the  subthalamic  region, 
disappearing  at  a  point  slightly  in- 
ferior to  the  level  of  the  red  nu- 
cleus. According  to  some  author- 
ities some  of  the  fibers  pass  from 
this  point  directly  through  the  in- 
ternal capsule  (peduncular  fibers), 
while  others  form  part  of  the  ansa 
lentiformis,  which  passes  trans- 
versely through  the  capsule.  The 
fillet  then  breaks  through  the  in- 
ternal limb  of  the  lenticular  nu- 
cleus, and,  ascending  in  the  poste- 
rior limb  of  the  capsule,  reaches 
the  cortex  of  the  posterior  central 
convolutions  and  of  the  parietal  lobe.  In  this  region  the 
fibers   of    the  neuron    undergo   their  terminal  divisions 


Fig.  19.  —  Schema 
showing  the  course  of 
the  sensory  pathway  :  J, 
In  the  cerebrum  and 
cerebral  peduncles  ;  //, 
pons  and  cerebellum  ; 
///,  medulla  oblongata  ; 
IV,  upper  portion  of  cer- 
vical cord  ;  T,  middle 
portion  of  cervical  cord  ; 
VI,  lumbar  cord  ;  a, 
fibers  from  the  antero- 
lateral columns  and  fil- 
let ;  6,  fibers  in  the  pos- 
terior columns  ;  c,  fibers 
from  cerebellum  and  lat- 
eral columns. 


THE  SENSORY  PATHWAY— SUPERIOR  FILLET.         55 

around  cells  situated  in  these  portions  of  the  cortex.  It 
is  probable  that  this  portion  is  interrupted  in  some  way  in 
the  globus  pallidus. 

Another  portion  of  the  superior  fillet  apparently  passes 
directly  from  the  subthalamic  region  to  the  internal  capsule, 
and,  ascending  in  the  posterior  limb  behind  the  pyramidal 
tract,  probably  ends  in  the  cortical  area  above  referred  to. 

According  to  another  description,  the  greater  part  or  even 
all  of  the  fibers  of  the  superior  fillet  are  interrupted  in 
the  ganglia  of  the  subthalamic  region,  the  globus  pallidus, 
and  especially  the  optic  thalamus  (in  the  lateral  basal  por- 
tion of  the  nucleus) — that  is  to  say,  the  superior  fillet  ends 
here.  According  to  this  view,  the  final  conduction  to  the 
cortex  would  necessitate  a  third  or  centrocortical  neuron 
(in  the  corona  radiata  of  the  optic  thalamus?),  but  our 
information  on  this  point  is  very  uncertain. 

2.  The  central  neurons  which  begin  in  the  cells  of  the 
posterior  horns  for  the  most  part  form  short  nerve  paths, 
most  of  which  end  within  the  spinal  cord.  Their  fibers 
enter  the  lateral  ground  bundle  of  the  same  side  (/  in  the 
serial  sections  shown  in  Plate  47)  and  the  ventral  portion 
of  the  posterior  column.  After  ascending  or  descending 
for  a  short  distance  they  reenter  the  gray  matter  and  break 
up  into  their  terminal  fibrils.  These  nerve  paths  are  then 
joined  by  others  of  similar  distribution,  so  that  con- 
duction is  effected  by  relays,  one  short  nerve  path  joining 
another. 

The  fibers  enter  the  substantia  reticularis  of  the  teg- 
mentum in  the  medulla  and  end  in  the  nuclei  situated  in 
this  region  (nucl.  lat.  post,  and  ant.  ?).  From  the  cells  of 
the  substantia  reticularis  (nucleus  magnocellularis)  fibers 
are  said  to  proceed  brain  ward  and  join  the  fillet. 

3.  Three  different  kinds  of  fibers  have  their  origin  in 
the  cells  of  tiie  middle  zone  in  the  spinal  cord,  forming 
shorter  and  longer  paths  : 

(a)  Ascending  fibers  which  enter  the  anterolateral  tract 
of  the  same  side.     Some  of  these  are  short  and  end  within 


56  THE  NEB  VO  US  PA  THWA  Y8. 

the  gray  matter;  others  continue  upward  and  reach  the 
substantia  reticularis  of  the  tegmentum,  where  they  join 
the  fillet — -fal  in  the  serial  sections. 

(6)  Ascending  fibers  which  enter  Gower's  column  of  the 
same  side,  and  continue  upward  as  far  as  the  medulla.  All 
the  longer  nerve  tracts  give  off  collateral  fibers  which  enter 
the  gray  matter  at  various  levels. 

Gower\s  column  in  part  also  enters  the  substantia  reticu- 
laris in  the  medulla.  Its  termination  within  the  mesen- 
cephalon, or  vermiform  process  of  the  cerebellum  (?),  is  still 
a  matter  of  dispute. 

(c)  Fibers  derived  from  the  median  groups  of  cells,  es- 
pecially in  the  anterior  horn,  so-called  commissural  cells, 
turn  inward  toward  the  median  line,  decussating  in  the 
anterior  commissure.  After  entering  the  anterior  horn  of 
the  opposite  side  they  ascend  on  this  side  with  the  fibers 
mentioned  under  (a),  forming  long  (?)  nerve  tracts.  In  the 
medulla  they  possibly  join  the  fillet  (probably  after  being 
interrupted  in  the  cells  of  the  substantia  reticularis  in  the 
tegmentum),  and  accompany  it  in  its  subsequent  course  to 
the  cortex. 

4.  From  the  cells  in  the  columns  of  Clarke  the  fibers 
of  the  central  pathway  enter  the  direct  cerebellar  tract  of 
the  same  side  (06  in  the  sections).  In  this  they  ascend 
and,  joining  the  restiform  body  in  the  medulla  at  its  ventral 
aspect,  accompany  this  structure  into  the  white  matter  of 
the  cerebellum  and  terminate  in  the  vermiform  process  (in 
the  tegmental  nucleus  of  the  opposite  side  ?). 

Such,  briefly  described,  is  the  course  of  the  sensory  cen- 
tral neurons  for  the  trunk  aud  extremities.  It  appears, 
therefore  that  a  part  of  these  neurons  passes  to  the  cortex 
directly  through  the  fillet  (decussating  in  the  decussation 
of  the  fillet),  while  another  part  passes  directly  to  the  cere- 
bellum through  the  direct  cerebellar  tract.  A  third  por- 
tion, chiefly  in  the  anterolateral  tract,  ascends  only  as  far  as 
the  substantia  reticularis  of  the  tegmentum  in  the  medulla 
oblongata  (some  of  them  undergoing  decussation  in  the  an- 


CONDUCTION  OF  SENSORY  IMPRESSIONS.  57 

terior  commissure).  From  this  point — that  is,  beginning  in 
the  nuclei  of  the  substantia  reticularis  (?) — we  must  assume 
another  centrocortical  neuron  for  the  conduction  to  the  cor- 
tex. A  part  of  these  fibers  (anterior  ground  bundle)  are 
said  to  join  the  superior  fillet ;  in  this  structure,  therefore, 
the  great  mass  of  the  central  sensory  neurons  eventually 
passes  to  the  cortex.  The  other  part  also  ascends  in  the 
substantia  reticularis  of  the  tegmentum,  at  least  as  far  as 
the  optic  thalamus. 

A  disputed  point  in  this  description  is  the  part  played 
by  the  decussation  in  the  anterior  commissure.  Many 
authors  deny  that  such  a  decussation  exists,  and  maintain 
that  there  is  only  a  direct  conduction  in  tlie  anterolateral 
tract.  The  posterior  commissure  also  contains  a  few  de- 
cussating fibers,  but  their  significance  is  not  well  under- 
stood. The  course  of  the  fillet  after  leaving  the  subthala- 
mic region,  or,  in  other  words,  of  that  portion  of  the 
superior  fillet  which  is  interrupted  in  the  thalamus,  is  also 
a  matter  of  dispute,  as  is  the  part  taken  by  the  ansa  lenti- 
formis,  as  well  as  various  other  points.  Compare  the  above- 
given  description  with  the  illustration  of  the  sensory  tracts 
in  Figure  20. 

As  regards  the  conduction  of  the  individual  qualities 
of  sensation,  the  following  arrangement  may  be  assumed 
as  the  probable  one  for  man,  judging  from  pathologic 
experience. 

Sensory  impressions  received  in  the  skin  and  deeper  soft 
portions  of  the  extremities  and  trunk  are  conducted  in  the 
peripheral  neuron  over  the  sensory  nerves,  spinal  ganglion 
cells,  and  posterior  roots,  into  the  spinal  cord.  It  is  not 
yet  definitely  decided  whether  the  various  qualities  of 
sensation  have  separate  tracts  in  this  part  of  their  course, 
but  it  seems  probable  that  they  have.  We  know,  for 
instance,  that  tactile  impressions  follow,  or  at  least  may 
follow,  a  different  course  than  impressions  of  temperature 
and  pain.  The  latter  are  conducted  by  the  pathways  that 
enter  the  posterior  horn,  and  must  continue  in  the  antero- 


58 


THE  NERVOUS  PATHWAYS. 


lateral   tract  (central   neuron).     Part  of   them    certainly 
undergo  decussation  (anterior  commissure?)  and  reach  the 

cortex,  and  hence  the  seat 
of  consciousness,  by  way 
of  the  fillet. 

The  tactile  sense  and 
the  muscle  sense  are  said 
to  reach  the  nuclei  of  Bur- 
dach  and  Goll  through 
the  long  tracts  in  the  pos- 
terior columns,  and  from 
there  by  the  nerve  path 
described  (internal  arcu- 
ate fibers),  the  fillet  of  the 
opposite  side,  by  which 
they  are  conducted  to  the 
cortical  center  of  con- 
sciousness. But  it  ap- 
pears that  for  the  tactile 
sense  at  least  conduction 
is  possible  through  other, 
shorter  paths, those  which 
have  been  described  as 
consisting  of  successive 
relays.  That  the  tactile 
sense  is  subsequently 
transmitted  in  the  fillet 
is  certain  (for  the  most 
part,  but  not  altogether, 
in  the  fillet  of  the  oppo- 
site side). 


^■^  S/iinalffcincflion 


juriph.Nertr. 


.  hint. 


•Ejiider 


t 


Fig.  20. — Schema  of  the  sensory  pathway:  Peripheral  neuron  (dotted 
line):  1,  2,3,  Short,  4,  long,  tracts.  The  ''switching  stations"  are 
indicated  by  small  circles.  Central  neuron  (broken  line):  /,  Columns 
of  Clarke  (direct  cerebellar  tract) ;  //,  interrupted,  77/,  long,  an- 
terolateral tracts,  i/.  Nuclei  of  posterior  column  (f.  gracilis  and 
f.  cuneatus)  ;  SIV,  decussatio  lemnisci ;  Schleife,  fillet;  hint.  ]Vurzel, 
posterior  root. 


SENSOBY  CRANIAL  NERVES.  59 

The  sensory  nerves  of  the  bladder,  rectum,  etc.,  enter 
the  spinal  cord  by  way  of  the  third,  fourth,  and  fifth  pos- 
terior sacral  roots,  their  peripheral  neurons  ending  in  the 
gray  matter  of  the  sacral  cord.  From  this  point,  or  per- 
haps higher  up  (long  ascending  fibers  of  the  posterior 
roots?),  the  central  conduction  possibly  begins  in  the  long 
tracts  of  the  posterior  columns  (columns  of  Goll  ?). 
ISTothing  definite  is  known  of  their  further  course  to  the 
higher  centers. 

Sensory  fibers  from  the  intestines  (peritoneum,  intestine, 
glands)  also  enter  the  sympathetic  plexuses,  especially  the 
splanchnic  plexus,  and  proceed  to  the  spinal  ganglia  and 
the  posterior  roots.  Their  subsequent  course  appears  to 
be  through  the  lateral  column  (cerebellar  lateral  tract  ?). 

The  tract  of  the  fillet  in 'the  tegmentum  contains  also 
the  central  neurons  for  the  various  sensory  cranial  nerves 
(except  the  olfactory  and  optic).  We  will  describe  them 
here  in  the  order  in  which  they  enter  from  below^  upward. 

1.  The  Sensory  Portion  of  the  Glossopharyngeo- 
vagus. — The  peripheral  neuron  fibers  run  in  tw^o  periph- 
eral nerves  to  the  cells  of  the  petrosal  and  jugular  ganglia, 
which  are,  therefore,  the  analogues  of  the  intervertebral 
ganglion  cells.  Emerging  from  these  in  the  corresponding 
nerve-roots,  they  pass  through  the  medulla  oblongata  and 
enter  the  sensory  glossopharyngeovagus  nucleus  in  the  pos- 
terior portion  of  the  floor  of  the  fourth  ventricle,  around 
the  cells  of  which  they  undergo  their  terminal  division. 
A  part  of  them,  instead  of  ending  in  this  region,  continue 
as  the  solitary  bundle  (fasciculus  solitarius,  or  descending 
root  of  the  glossopharyngeovagus)  for  a  short  distance 
downward,  and  end  around  cells  in  the  neighborhood  of 
this  nucleus  (posterior  horn). 

The  central  neuron  originates  in  these  cells  and  in  the  cells 
of  the  sensory  nucleus.  It  runs  toward  the  raphe,  crosses 
to  the  other  side  at  this  point,  and  joins  the  median  or 
superior  tract  of  the  fillet  (described  as  the  "  scattered  bun- 
dle "  of  the  fillet).     Together  with  the  superior  fillet  the 


60  THE  NEB  VO  US  FA  THWA  YS. 

central  neuron  complex  continues  its  way  toward  the  cor- 
tex, lying  behind  the  pyramidal  fibers  in  the  internal  cap- 
sule, and  undergoes  its  terminal  division  around  the  cor- 
tical cells  near  the  termini  of  the  fillet  (posterior  central 
convolution  (?)  for  the  fibers  of  taste  in  the  base  of  the 
lower  frontal  convolution  (?) ). 

2.  Sensory  Portion  of  the  Trigeminus. — Its  peripheral 
neuron  fibers,  after  emerging  from  the  three  sensory 
branches  of  the  fifth  nerve,  enter  the  cells  of  the  Gasse- 
rian  ganglion  and  emerge  on  the  other  side  as  the  posterior 
root.  After  passing  through  the  fibers  of  the  pons  they 
terminate  around  the  cells  of  the  sensory  nucleus  of  the 
trigeminus.  Some  of  the  fibers  descend  for  some  distance 
to  the  upper  portion  of  the  cervical  cord  as  the  descending 
(caudal  Vc)  root  of  the  fifth  nerve,  formerly  erroneously 
called  the  ascending  root,  and  are  gradually  lost.  This 
descending  root  of  the  fifth  nerve  can  be  seen  in  any 
transverse  section  of  the  medulla  oblongata,  lying  on  the 
outer  side  of  the  remains  of  the  posterior  horn,  the  sub- 
stantia reticularis  of  the  tegmentum,  the  upper  extremity 
of  which  forms  the  sensory  nucleus  of  the  trifacial.  The 
"  nasal  root  ^-  of  the  fifth  nerve,  described  above  as  a  motor 
root,  was  formerly  regarded  as  a  sensory  root ;  its  signifi- 
cance is  not  quite  clear.  If,  as  seems  probable,  it  is  motor 
in  character,  it  should  also  be  designated  descending.  Fin- 
ally, a  third  portion  is  said  to  pass  directly  from  the  sen- 
sory root  of  the  trifacial  nerve  to  the  cerebellum  (direct 
sensory  cerebellar  tract).  On  this  supposition  it  should, 
therefore,  be  regarded  as  an  analogue  of  the  cerebellar 
lateral  tract  of  the  cord. 

The  central  neuron  originates  in  the  cells  of  the  sensory 
nucleus,  situated  in  the  immediate  neighborhood  of  the 
descending  root.  The  fibers,  after  decussating  in  the 
raphe  of  the  tegmentum,  join  the  superior  fillet  (scattered 
bundle)  and  accompany  the  latter  toward  the  cortex  (pos- 
terior central  convolution),  where  they  undergo  their  ter- 
minal division. 


SENSOEY  CRANIAL  NERVES.  61 

3.  The  Auditory  Nerve. — The  auditory  nerve  sub- 
divides into  two  branches  possessing  distinct  functions,  the 
cochlear  and  the  vestibular  nerves. 

(a)  The  cochlear  nerve  is  the  true  nerve  of  hearing. 
The  peripheral  neuron  begins  in  the  organ  of  Corti  in 
the  cochlea,  and  enters  the  cells  of  the  cochlear  ganglion, 
an  analogue  of  the  intervertebral  ganglia,  also  situated 
within  the  cochlea.  [Note. — The  peripheral  neuron  be- 
gins in  the  cells  of  the  spiral  ganglion,  in  the  bony  walls 
of  the  cochlea,  and  passes  outward,  terminating  about  the 
organ  of  Corti  in  the  cochlear  duct.  The  spiral  ganglion 
is  an  analogue  of  the  intervertebral  ganglia. — E.  D.  F.] 
After  emerging  from  the  cochlear  ganglia  it  enters  the 
medulla  as  the  cochlear  nerve,  and  undergoes  its  terminal 
division  about  the  cells  of  the  ventral  auditory  nucleus, 
embracing  the  restiform  body  on  each  side.  At  this  point 
the  central  neuron  begins  as  the  trapezoid  body  underneath 
the  tegmentum  and  the  striae  acustica  above  the  tegmen- 
tum of  the  medulla,  and  runs  to  the  raphe,  where  decus- 
sation takes  place.  It  then  continues  in  the  lateral  inferior 
fillet  of  the  corpora  quadi'igemina,  which  is  situated  to  the 
outer  side  of  the  mesial  or  superior  fillet.  Some  of  the 
fibers  do  not  cross  to  the  other  side,  but  pass  to  the 
lateral  fillet  of  the  same  side,  and  come  into  relation  with 
the  superior  olive  through  fibers  of  the  trapezoid  body. 
The  lateral  fillet  is  continued  to  a  point  beneath  the  cor- 
pora quadrigemina  at  the  region  indicated,  and  ends  partly 
in  the  posterior  quadrigemina  and  partly,  through  the  pos- 
terior brachium,  in  the  median  geniculate  body  ;  here  it  is 
joined  by  a  third  centrocortical  tract  (?).  From  this  point 
it  is  supposed,  on  clinical  grounds,  that  the  central  audi- 
tory pathway  continues  to  the  subthalamic  region  and 
thence  to  the  posterior  limb  of  the  internal  capsule,  be- 
hind the  above-described  direct  sensory  (superior)  fillet 
fibers  of  the  internal  capsule.  From  the  capsule  the  fibers 
pass  to  the  cortex  of  the  superior  temporal  convolution, 
especially  to  its  posterior  third. 


62  THE  NEE  VO  US  PA  THWA  Y8. 

(b)  The  Vestibular  Nerve. — The  peripheral  neuron  orig- 
inates where  the  neuron  cells  are  situated,  in  the  semicir- 
cular canals  of  the  labyrinth,  and  undergoes  its  terminal 
division  about  the  cells  of  the  dorsal  auditory  nucleus  and 
neighboring  groups  of  cells  (Deiters'  nucleus),  at  the  lateral 
margin  of  the  floor  of  the  fourth  ventricle.  [Note. — The 
peripheral  neuron,  which  has  its  origin  in  the  vestibular 
ganglion  (intumescentia  gangliformis  of  Scarpa)  situated 
within  the  auditory  meatus,  is  divided  into  two  portions — 
an  external  and  an  internal  portion.  The  external  portion 
of  the  neuron  passes  from  the  ganglion  and  terminates 
about  the  fusiform  cells  in  the  semicircular  canal.  The 
internal  portion  passes  dorsally,  and  terminates  about 
the  dorsal  auditory  nucleus  and  neighboring  groups  of 
cells  (Deiters'  nucleus)  at  the  lateral  margin  of  the  floor 
of  the  fourth  ventricle.]  Part  of  the  fibers  unite  to  form 
the  descending  root  of  the  eighth  nerve,  while  others 
ascend  to  the  cerebellum  as  the  direct  sensory  cerebellar 
tract.  From  the  sensory  nucleus  the  central  neuron  (trap- 
ezoid body)  passes  up  to  the  (mesial  ?)  fillet,  and  so  to  the 
cortex,  after  undergoing  decussation  in  the  raphe.  The 
cortical  area  is  not  known. 

The  course  of  the  optic  and  olfactory  nerves  differs  from 
that  of  the  sensory  nerves,  which  we  have  described  so  far. 
In  fact  they  are  not  to  be  regarded  as  peripheral  nerves, 
but  as  modified  portions  of  the  cerebrum,  as  appears  from 
an  examination  of  their  structure  and  development. 

4.  Optic  Nerve. — The  peripheral  neuron  is  situated  en- 
tirely within  the  external  layers  of  the  retina.  The  central 
neuron  begins  in  the  internal  ganglion  layer  of  the  retina, 
the  neuron  fiber  in  its  centripetal  course  being  contained  in 
the  optic  nerve.  A  partial  decussation  takes  place  in  the 
chiasm  in  such  a  way  that  the  fibers  from  the  left  half  of 
each  retina  come  to  lie  within  the  left  optic  tract,  and  those 
from  the  right  halves  in  the  right  optic  tract.  Thus  the 
fibers  from  the  nasal  halves  of  both  retinae,  comprising 
two-thirds  of  the  entire  optic  nerve,  undergo  decussation. 


SENSOEY  CRANIAL  NEBVES,  63 

It  follows  that  each  optic  tract  contains  fibers  from  both 
optic  nerves,  representing  both  long  and  short  nerve  tracts. 
The  long  nerve  tracts  run  within  the  optic  tract  to  the 
lateral  geniculate  body,  which  they  encircle,  and  pass 
directly  to  the  adjoining  posterior  limb  of  the  internal 
capsule,  occupying  its  most  posterior  portion,  and  eventu- 
ally terminate  in  the  occipital  lobe  (Gratiolet's  optic  radia- 
tion). The  existence  of  these  direct  fibers  has  been  dis- 
puted, and  not  without  good  reason.  The  short  nerve 
tracts,  which  are  undoubtedly  by  far  the  more  numerous, 
undergo  their  terminal  division  in  the  cells  situated  about 
the  primary  optic  centers  (lateral  geniculate  body,  anterior 
corpus  quadrigeminum,  and  pulvinar).  From  these  cells 
a  third  centrocortical  neuron,  consisting  of  the  nerve-fibers 
of  these  cells,  joins  the  optic  radiation  in  the  posterior 
limb  of  the  capsule,  and  passes  to  the  cortex  of  the  occip- 
ital lobe  (cuneus).  Here  the  fibers  from  both  nerve  tracts 
undergo  their  terminal  division. 

The  optic  tract  also  contains  fibers  derived  from  the 
anterior  corpus  quadrigeminum,  which,  for  the  most  part, 
undergo  decussation  and  pass  centrifugally  to  the  retina 
(descending  optic  fibers).  Their  significance  is  not 
clear. 

5.  Olfactory  Nerve. — The  peripheral  neuron  is  repre- 
sented by  the  olfactory  nerves  which  begin  in  the  special- 
ized epithelial  cells  of  the  membrana  olfactoria,  the  ana- 
logues of  spinal  ganglion  cells.  These  nonmedullated  fibers 
go  to  the  olfactory  bulb  and  terminate  around  the  cells 
situated  in  that  structure,  which  form  the  olfactory  glo- 
meruli. From  this  point  the  central  rzeitron  (mitral  cells) 
continues  within  the  olfactory  tract.  Some  of  the  fibers 
undergo  decussation  in  the  anterior  commissure,  while 
others  pass  directly  to  the  cortex  in  the  gyrus  fornicatus 
and  gyrus  hippocampi.  (The  fornix,  corpora  albicantia, 
and  various  bundles  of  fibers  in  the  thalamencephalon  also 
form  part  of  the  ^^ olfactory  fibrillation"  and  its  associa- 
tion bundles.) 


64  THE  NERVOUS  PATHWAYS. 

As  in  the  case  of  the  motor  nerve  tract,  the  central 
neuron  for  the  most  part  undergoes  decussation,  while  the 
peripheral  neuron  does  not.  (See  Fig.  18.)  Hence  most 
impressions  are  conveyed  to  the  cortex  of  the  opposite 
hemisphere,  and  only  a  smaller  part  to  the  cortex  of  the 
same  hemisphere,  again  resembling  the  conditions  in  the 
motor  tract.  However,  the  proportion  of  fibers  going  to 
the  hemisphere  of  the  same  side  is  greater  in  the  sensory 
than  in  the  motor  pathway. 

We  now  turn  to  the  discussion  of  the  connections  be- 
tween the  motor  and  the  sensory  pathways. 

Both  the  peripheral  motor  and  sensory  neurons  and  the 
central  motor  and  sensory  neurons  are  physiologically  con- 
nected with  each  other,  the  connection  between  the  former 
being  known  as  the  reflex  path,  that  between  the  latter  as 
the  pathway  of  conscious  volitional  reaction. 

(a)  The  Reflex  Paths.  —  By  a  reflex  we  mean  a 
motor  act  performed  automatically  (nonvolitionally)  in 
response  to  a  sensory  impression.  The  entire  act  is  con- 
fined to  the  peripheral  neurons,  ^  which,  therefore,  form 
the  reflex  tract  (reflex  arc).  The  reflex  arc  is  composed 
of  a  sensory  portion  contributed  by  the  sensory  peripheral 
neuron,  a  motor  portion  contributed  by  the  motor  periph- 
eral neuron,  and  a  connecting  link  formed  by  a  branch 
of  the  sensory  neuron  after  its  entrance  into  the  spinal  cord 
or  brain-stem.  The  latter  is  known  as  the  reflex  coUatei^al, 
and  has  been  described  on  page  51  as  the  short  process 
of  the  posterior  spinal  roots  passing  to  the  motor  cells  in  the 
anterior  horn  (under  5).  The  reflex  tracts  become  med- 
ullated  very  early  in  fetal  life,  in  accordance  wdth  the 
well-known  fact  that  the  first  movements  of  the  embryo 
are  reflex  in  nature. 

1.  The  Cutaneous  and  Tendon  Reflex  Arcs.  —  The 
course  of  these  reflex  arcs  is  better  known  than  that  of 
any  other.     The  sensory  portion  is  formed  by  the  periph- 

^  It  is  still  undecided  whether  any  reflex  paths  exist  in  the  sympa- 
thetic nerve  (reflex  center  in  the  ganglia  of  the  sympathetic). 


THE  REFLEX  PATHS.  '66 

eral  sensory  neuron,  the  connecting  branch  by  the  reflex 
collaterals  which  ramify  among  the  cells  of  the  anterior 
horn.  It  is  probable  that  only  a  part  of  the  cells  in  the 
anterior  horn  are  concerned  in  this  reflex.  We  distin- 
guish a  short  and  a  long  reflex  arc. 

(a)  The  short  reflex  arc  consists  of  a  collateral  which 
passes  directly  from  the  posterior  column  through  the  pos- 
terior horn  to  the  cell  in  the  anterior  horn  (plantar  reflex, 
patellar  reflex,  spinal  reflexes). 

(6)  The  long  reflex  arc  is  formed  by  the  reflex  collateral 
splitting  up  about  a  cell  in  the  anterior  horn.  From  this 
cell  an  ascending  and  a  descending  branch,  with  several 
collaterals,  pass  to  one  or  more  motor  ganglion  cells  which 
may  be  situated  at  various  levels  of  the  anterior  horn  and 
brain-stem.  This  gives  the  possibility  of  reflex  move- 
ments being  transmitted  to  more  remote  muscle  groups. 
Tlie  fibers  of  the  posterior  longitudinal  bundle  appear  to 
be  concerned  in  this  function  (reflex  transmission  of  sensory 
impulses  to  the  movements  of  the  eye). 

The  localization  of  some  of  the  reflexes  belonging  to 
this  group  is  seen  in  Plate  13.  (For  more  detailed  de- 
scription see  Part  IV,  3.) 

2.  The  Complicated  Reflex  Arcs. — We  have  very  lit- 
tle definite  knowledge  of  the  course  of  these  reflexes.  The 
pharyngeal,  na^al,  and  bronchial  reflex  arc  is  composed  of 
sensory  fibers  from  the  trifacial,  glossopharyngeal,  and 
pneumogastric  nerves  and  the  corresponding  motor  nerves, 
the  pneumogastric  and  spinal  accessory. 

The  conjunctival  reflex  is  composed  of  fibers  from  the 
trigeminal  and  facial  nerves. 

The  pupillary  reflex  is  composed  of  fibers  from  the  optic 
and  oculomotor  nerves  (corpora  quadrigemina — oculomo- 
tor nucleus  ?).  The  reflex  collaterals  evidently  pass  from 
the  sensory  nerves  to  the  corresponding  motor  nuclei.  It 
is  supposed  that  the  cortex  is  also  included  in  some  of 
these  reflex  arcs.  We  are  still  without  any  sufficient  data 
for  the  localization  of  other  important  reflexes  connected 
5 


6  6  THE  NEE  VO  US  PA  THWA  VS. 

with  the  auditory,  optic,  and  other  nerves.      (For  a  de- 
tailed description  of  these  reflexes  see  Part  IV,  4.) 

The  reflexes  for  the  functions  of  the  bkidder  and  rec- 
tum are  situated  in  the  sacral  cord.  (See  sensory  and 
motor  paths  for  these  organs.) 

(b)  The  Volitional  Pathways. — Superimposed  above 
the  reflex  arc,  which  is  composed  of  the  two  peripheral  neu- 
rons, there  is  a  second  arc,  formed  by  the  central  sensory 
and  motor  neurons  and  their  connecting  fibers  in  the  cere- 
bral cortex.  This  arc  effects  the  transmission  of  a  con- 
scious sensory  impulse  to  a  volitional  motor  act. 

At  the  same  time  the  central  motor  neuron  exercises  an 
inhibitory,  and  the  sensory  central  neuron  a  controlling, 
influence  on  reflex  processes. 

All  conscious  processes  are  enacted  in  the  cerebral  cortex, 
in  which  the  sensory  nerve  tracts  end  and  the  motor  nerve 
tracts  begin.  The  cerebral  cortex  also  contains  the  con- 
necting fibers  between  the  motor  and  sensory  portions  of 
the  cortex.  It  is  improbable,  although  conceivable,  that 
the  sensory  neuron  fibers  terminate  directly  about  the 
motor  ganglion  cells ;  it  is  more  likely  that  one  or  more 
neurons  of  another  kind  (transcortical)  are  interposed. 
(See  the  schema  on  Plate  17.) 

A  study  of  the  development  of  the  fetal  and  childish 
psychic  activity  affords  an  approximate  idea  of  the  char- 
acter of  conscious  processes  in  the  cerebellar  cortex. 
Although  it  does  not  actually  begin  until  after  birth,  yet  a 
series  of  sensory  and  reflex  processes  are  enacted  even 
during  intra-uterine  life. 

The  first  movements  are  undoubtedly  reflex  in  charac- 
ter, since,  as  has  been  already  stated,  the  reflex  arcs  early 
assume  a  medullary  sheath.  Since  the  fibers  in  the  teg- 
mentum (fillet)  become  medullated  long  before  those  in 
the  central  motor  tracts,  it  is  evident  that  there  is  a  pri- 
mary transmission  of  sensory  impressions  from  the  entire 
periphery  of  the  body  to  the  cerebral  cortex,  especially  the 
posterior  central  convolution  and  the  parietal  lobe,  forming 


THE  VOLITIONAL  PATHWAYS— IDEATION.  67 

the  basis  for  the  volitional  activity  that  develops  later. 
The  neurons  and  neuron  complexes  situated  in  these  areas 
possess  the  peculiar  property  of  permanently  preserving 
these  sensory  impressions  as  memory  pictures,  and  repro- 
ducing them  later  under  certain  conditions.  In  this  they 
are  assisted  by  the  primary  association  processes  (connec- 
tions with  other  cortical  neurons,  and  corresponding  chemic 
and  physical  processes  in  the  structure  of  the  neurons  ?). 

After  the  child  is  born,  another  set  of  memory  pictures, 
produced  by  the  sound-waves  that  reach  the  upper  tem- 
poral convolution  through  the  lateral  auditory  fillet,  are 
stored  up.  In  like  manner  also  are  stored  up  the  visual 
impressions  which  pass  through  the  optic  radiation  and  are 
deposited  in  the  occipital  lobe,  especially  in  the  cortex  of 
the  cuneus  and  in  the  gray  matter  surrounding  the  calca- 
rine  fissure.  In  addition  there  is  a  similar  storing-up  of 
olfactory  and  gustatory  impressions. 

These  groups  of  memory  pictures,  which,  as  we  have 
seen,  are  localized  in  different  portions  of  the  cortex,  are 
connected  by  means  of  tlie  secondary  association  processes 
with  each  other  and  with  memory  pictures  in  the  hemi- 
spheres both  of  the  same  (association  tracts  in  the  stricter 
sense)  and  of  the  opposite  side  (commissural  fibers).  Thus 
each  individual  })sychic  process  is  associated  with  a  distinct 
complex  of  specially  trained  neurons,  belonging  both  to 
the  projection  and  association  fibrillation  ;  these  associated 
and  cooperating  neuron  articulations  may  be  designated  as 
neuron  elements. 

It  is  by  means  of  these  association  processes  between 
the  neuron  elements  that  ideation  takes  place.  Every  idea 
or  concept  consists  of  a  collection  of  associated  memory 
pictures.  The  higher  associations  form  the  ideas,  and  the 
connection  between  these  higher  associations  gives  rise  to 
logical  mental  processes.  The  reproduction  of  this  asso- 
ciation is  called  a  concept.  Only  a  part  of  all  the  associa- 
tions is  actively  engaged  at  any  definite  time,  the  other 
part  remaining  dormant.     The  organ  of  the  intellect  is, 


6  8  THE  NEB  VO  US  PA  THWA  VS. 

therefore,  the  association  fibrillation.  The  sum  of  the  ac- 
tive associations  plus  the  newly  arrived  sensory  impres- 
sions make  up  the  greater  part  of  the  contents  of  conscious- 
ness.    Hence  consciousness  is  subject  to  continual  change. 

It  is  probable  that  a  considerable  portion  of  the  associa- 
tion fibers  are  concerned  in  what  is  known  as  subcon- 
sciousness (unconscious  associations).  In  addition  to  the 
above-named  sensory  impressions  there  is  another  set  of 
impressions  which  reach  the  cerebral  cortex  and  which  are 
worked  up  into  unconscious  associations.  These  include 
the  muscular  and  articular  impressions  which  are  con- 
ducted toward  the  center  in  the  early  reflex  processes. 
They  are  deposited  in  the  central  convolutions,  probably 
in  the  immediate  vicinity  of  the  motor  centers,  and  form 
the  so-called  innervation  feelings,  produced  by  the  muscular 
activity  of  the  various  motor  acts  (kinesthetic  memory 
pictures). 

By  the  reproduction  of  these  memory  pictures  of  inner- 
vation— feelings  which  are  deposited  in  postfetal  life  and 
connected  with  each  other  by  unconscious  associations — 
conscious  volitional  muscular  activity  is  in  some  way  made 
possible  and  subjected  to  the  necessary  control.  A  voli- 
tional movement  is,  therefore,  merely  the  external  expres- 
sion of  certain  concepts.  The  path  by  which  the  impres- 
sions are  transmitted  from  the  endings  of  the  sensory  cen- 
tral neurons  to  those  of  the  central  motor  neurons,  which 
must  be  situated  in  the  cortex,  is  the  true  analogue  of  the 
reflex  collaterals  of  the  peripheral  neurons. 

Perhaps  an  example  will  serve  to  illustrate  the  foregoing 
discussion.  On  Plate  17,  Figure  3,  we  see  the  reflex  arc  :  the 
sensory  portion,  sp  (brown),  the  reflex  portion,  r,  the  motor 
portion,  mp  (blue).  Above  the  reflex  arc  we  see  the  cen- 
tral tract  for  conscious  actions  :  the  sensory  portion  (green), 
the  connecting  neuron  (black),  and  the  motor  portion  (red). 
The  memory  pictures  of  the  special  sense  impressions  and 
muscular  sensations  are  deposited  around  the  sensory 
(green)  fibrillations  in  the  cortex — that  is  to  say,  in  the 


SPEECH  CENTERS.  69 

commissural  and  association  neurons  of  the  cortex  (black) 
which  go  to,  and  come  from,  other  areas  in  the  cortex. 

If  the  toe  is  irritated,  there  is  a  reflex  twitching  in  the 
corresponding  leg  (reflex  arc  from  the  brown  neuron  to  the 
blue,  reflex  transmission  in  the  lumbar  cord)  ;  at  the  same 
time  the  sensory  irritation  is  transmitted  by  means  of  the 
green  neuron  to  the  cortex,  where  it  becomes  associated 
with  various  mental  pictures  and  produces  the  well-known 
sensation  of  pain.  As  a  second  irritation  is  threatened 
(association  with  recent  optic  impressions),  the  painful  sen- 
sation sends  a  message  through  the  motor  tracts  (red- blue) 
necessary  for  the  movement  of  the  leg,  by  means  of  the 
corresponding  innervation  feelings  (paracentral  lobule), 
which  convey  the  impulse  to  the  muscles  they  supply. 

Among  the  various  cortical  activities  that  are  set  in 
motion  in  this  way  we  are  chiefly  interested  in  the  act  of 
speech.  As  the  child  learns  to  speak  the  sound  pictures 
of  the  words  that  it  hears  are  deposited  in  the  superior 
temporal  convolution  of  the  left  hemisphere  (word-sound 
center,  sensory  speech  center).  In  order  to  understand  the 
meaning  of  the  sound  pictures  (their  interpretation)  the 
associative  activity  by  which  they  are  encompassed  is 
necessary. 

The  sensory  speech  center  is  connected  by  means  of  the 
fasciculus  uncinatus  with  the  motor  speech  center,  which  is 
situated  at  the  base  of  the  inferior  frontal  convolution  on 
the  left  side  (Broca's  convolution).  In  this  area,  or  at 
least  in  its  immediate  neighborhood,  the  innervation  feel- 
ings (kinesthetic  memory  pictures)  of  all  the  muscular 
movements  necessary  for  the  act  of  speech  (tongue,  mouth, 
palate,  larynx)  are  deposited  by  constant  exercise  and  imi- 
tation. The  production  of  these  movements  in  response 
to  an  impulse  from  the  sensory  speech  center  ultimately 
leads  to  the  complicated  muscular  acts  necessary  for  the 
production  of  letters,  words,  and  sentences.  If  by  any 
accident  the  hearing  of  the  child  is  destroyed,  the  power 
of  learning  to   speak   is   necessarily   lost  and  the   child 


70 


THE  NEB  VO US  PA THWA  Y8. 


becomes  a  deaf  mute.  The  processes  that  go  on  while  the 
child  is  learning  to  speak  are  constantly  accompanied  by 
association  processes  with  memory  pictures  in  other  centers, 
especially  visual  and  tactile  images.  The  greater  the 
number  of  images  stored  up  in  the  cortex,  and  the  more 
effective  the  associations  between  them,  the  greater  will  be 
the  intellectual  capacity  of  the  brain  in  question.  The 
speech  centers,  like  those  which  preside  over  reading  and 
writing  and  which  will  be  discussed  below,  are  found  only 
in  one  hemisphere — in  the  left  hemisphere  in  right-handed 
people,  usually  in  the  right  hemisphere  in  left-handed 
people.  The  motor  speech  center  is  probably  identical 
with  the  centers  of  the  facial,  hypoglossus,  etc.  The  speech 
tract  (see  p.  47)  connects  these  centers  in  the  left  hemi- 


Fig.  21. 


sphere  with  the  nuclei  of  the  seventh,  twelfth,  and  other 
nerves  on  both  sides  of  the  brain. 

When  the  child  learns  to  read,  the  graphic  memory 
pictures  are  deposited  in  the  visual  center  in  the  occipital 
lobe  (the  interpretation  of  written  speech  is  lodged  princi- 
pally in  the  angular  gyrus).  They  reach  the  conscious- 
ness, however,  only  by  association  with  the  auditory  center 
and  with  the  motor  speech  center,  because,  in  learning  to 
read,  the  graphic  image  is  always  converted  into  an  audi- 
tory image  and  into  a  motor  speech  image  (reading  aloud). 
In  later  life  many  people  are  more  and  more  able  to  dis- 
pense with  these  association  processes. 

In  learning  to  read,  the  graphic  images  are  deposited  as 
innervation  feelings  of  the  movements  concerned  in  writ- 


SPEECH,    WRITING,  ETC.  71 

ing  in  the  center  for  the  right  arm,  and  in  the  adjoining 
posterior  third  of  the  middle  frontal  convolution.  ^  They 
become  intimately  associated  with  visual  and  auditory 
images  on  that  side  of  the  brain ;  therefore,  the  motor 
graphic  images  of  the  letters  are  produced  before  the 
visual  images. 

In  some  individuals  the  visual  graphic  associations  are 
more  prominent,  while  in  others  the  kinesthetic  associa- 
tions are  better  developed.  Hence  the  cortical  areas  in 
which  these  processes  are  enacted  are  the  central  convolu- 
tions, the  superior  temporal  convolution,  and  the  convolu- 
tions of  the  parietal  and  occipital  lobe.     The  frontal  lobe 


peulus   J 


lutftut 


braehuj 


is  regarded  as  the  anatomic  basis  of  the  higher  intellectual 
functions.  But  it  is  to  be  remembered  that  the  compli- 
cated processes  by  which  we  are  enabled  to  think  necessi- 
tate very  complex  associations,  the  sum  of  which  can  not 
possibly  be  confined  to  the  activity  of  a  single  lobe. 

It  is  seen  by  Figure  21  that  the  left  hemisphere  is  the 
more  important  as  regards  the  distribution  of  the  centers. 
The  ^'  latent  ^^  cortical  areas  are  white.  The  dotted  areas 
correspond  with  the  psychosensory  and  psychomotor  areas, 

1  Some  authorities  place  the  writing  center  in  the  inferior  parietal 
lobule. 


7  2  THE  NEE  VO  US  PA  THWA  YS. 

projection  tracts  and  association  tracts,  while  the  other 
convolutions  of  the  cortex  (white)  are  said  to  contain  ex- 
clusively association  fibers.  (For  the  details  see  Plate  21.) 
Figure  22  is  intended  to  illustrate  the  processes  con- 
cerned in  the  acts  of  speech,  writing,  etc.  The  connec- 
tions effected  in  speaking,  writing,  and  reading  are  seen  in 
the  following  scheme : 

1.  Sensory  speech  tract     .    ,    .    ,        .      I  center. 

2.  Motor  speech  tract       II  center. 

3.  Optic  tract Ill  center. 

4.  Kinesthetic  tract  for  movements 

required  in  speaking  and  writing  IV  center. 

5.  Motor  tract  for  writing V  center  (center  for  the  arm). 

By  X  we  will  designate  the  ideation,  which  is  not  re- 
garded as  bound  to  a  particular  center,  but  rather  as  the 
effect  of  the  entire  associative  activity.  A  part  of  the 
more  important  associations  is  added  (as  a). 

X 

Learning  to  speak  :   1  (a  3)  —  I  —  II  (a  IV)  —  2. 

X 

Learning  to  read  :   3  —  III  —  rfo^IV)  —  II  —  2. 

X 

Learning  to  write  :   3  —  III  —  I  {a  IV,  a\\)  —  V  —  5. 
Spontaneous  speech  :  x  —  II  («  IV,  a  I)  —  2. 

X 

Spontaneous  reading  :   3  —  III  —  I  (a  IV)  —  II  ^  2. 
Spontaneous  writing  :  x  —  I  ( II)  —  III  — V  (alV)  —  5. 
Imitative  speech  i :  1  —  I—  II  (rt  IV)  —  2. 
Imitative  writing  :  3  —  III  —  V  («  IV)  —  5. 
Writing  from  dictation  :  1  —I  (a  III)  —  V  (a  IV)  —  5. 

To  avoid  repetition,  any  further  important  particulars 
in  regard  to  the  physiology  of  other  portions  of  the  brain 
will  be  referred  to  under  the  head  of  General  Symptom- 
atology, Part  IV,  3,  Topical  Diagnosis. 

A  word  in  regard  to  the  coordination  of  motor  acts. 
Even  the  slightest  motor  act  necessitates  the  cooperation 

^  If  mechanical,  without  concept  associations  (x). 


COORDINATION.  73 

of  sev^eral  muscle  groups.  The  regulation  of  the  proper 
working  of  the  various  muscles  concerned  in  any  simple 
or  complicated  act  is  called  coordination. 

Even  a  very  simple  muscular  act  requires  the  coordi- 
nation of  antagonistic  muscles ;  how  much  more  then  the 
complex  motor  processes  made  up  of  a  succession  of  dif- 
ferent single  acts,  such  as  walking,  speaking,  etc.,  where 
not  only  each  individual  motor  act,  but  also  the  proper 
chronologic  succession,  requires  careful  regulation. 

Cooperating  muscle  groups  derive  their  peripheral  and 
probably  also  their  central  neurons,  or  at  least  a  part  of 
them,  from  cells  that  are  intimately  connected  with  each 
other  (coordination  centers  and  coordination  tracts  of  the 
brain  and  spinal  cord).  Thus  the  nuclei  of  the  ocular 
muscles  and  the  nuclei  of  the  hypoglossus  are  very  inti- 
mately connected.  Even  a  single  cell  may  send  out  through 
the  collaterals  motor  impulses  to  various  muscles,  and 
thereby  assist  in  the  coordination  of  the  muscular  act. 

The  sensoi^  impressions,  especially  impressions  of 
muscular  sense,  play  an  important  part  in  coordination, 
and  it  still  remains  to  speak  of  this  controlling  influence  and 
of  the  influence  of  the  cerebellum  on  static  coordination. 

There  is  no  doubt  that  the  cerebellum  exercises  an  influ- 
ence on  the  static  coordination  and  equilibrium  of  the  body 
in  the  erect  position  and  while  walking.  For  this  purpose 
it  receives,  through  centripetal  nerve  tracts,  the  impressions 
of  muscular  sense,  and  optic,  tactile,  and  other  impressions 
from  the  periphery  of  the  body.  That  portion  of  the  pos- 
terior column  which  does  not  join  the  fillet  makes  its  way 
from  the  nuclei  in  the  posterior  cord  through  the  restiform 
bodies  to  the  cerebellum.  We  further  know  that  the  cere- 
bellum receives  fibers  through  the  cerebellar  lateral  tract 
(function  unknown),  from  the  vestibular  nerve  (semicir- 
cular canals — organ  of  equilibrium?)^  and  from  the  tri- 
geminus (direct  sensory  cerebellar  tract).  In  the  inter- 
pretation of  the  cerebellar  influence  on  coordination, 
however,  we  are  still  in  the  speculative  stage. 


74  THE  NEB  VO  US  PA  THWA  VS. 

As  the  cerebellum  possesses  various  connections  with 
the  cerebrum,  it  is  quite  conceivable  that  it  may  exert 
some  controlling  influence  on  the  motor  centers  in  the  cor- 
tex, and,  therefore,  indirectly  on  muscular  activity.  But, 
unfortunately,  it  does  not  appear  to  be  directly  connected 
with  these  centers. 

The  fibers  of  the  pons  connect  the  cerebellum  with  the 
ganglia  in  the  opposite  side  of  the  pons,  where,  as  we  have 
seen,  both  the  frontal  and  the  temporo-occipital  pontal 
tract  terminate.  It  appears,  therefore,  that  each  hemis- 
phere of  the  cerebellum  is  in  direct  communication  with 
the  frontal,  temporal,  and  occipital  lobes  of  the  opposite 
cerebral  hemisphere. 

In  addition,  there  is  a  communication  by  means  of  the 
brachium  between  the  red  nucleus  of  the  tegmentum  (which 
in  turn  is  connected  with  the  optic  thalamus,  etc.)  and  the 
opposite  hemisphere  of  the  cerebellum.  Although  these 
connections  between  the  cerebellum  and  cerebrum  are  well 
known,  their  functions  are  not  understood,  but  it  may  be 
said  that  they  appear  to  be  in  some  way  associated  with 
coordination. 

There  is  some  anatomic  basis  for  the  theory  that  the 
muscles  are  directly  influenced  by  the  cerebellum.  The 
cerebellum  is  connected,  by  means  of  the  olivary  fibers 
in  the  restiform  body,  with  the  olive  of  the  opposite  side, 
and  from  this  point  the  central  tegmental  tract  (mesial 
fillet)  is  continued  upward,  while  the  "olivary  tracts'' 
descend  in  the  lateral  column  to  cells  in  the  anterior 
horn  (?).  When  all  is  said,  however,  we  must  admit  that 
we  have  no  definite  knowledge  on  this  point. 

It  remains  to  be  mentioned,  in  regard  to  the  cerebellum, 
that  it  does  not  contain  any  separate  centers  like  those  in 
the  cerebrum.  Any  one  part  of  the  cerebellum  can  be 
supplied  by  another.  In  general  it  may  be  said  tliat  it  is 
credited  with  a  stcUiCf  tonic,  and  sthenic  influence  on  mus- 
cular activity. 


PART   IV. 

GENERAL  PATHOLOGY  AND  TREAT- 
MENT  OF  DISEASES  OF  THE  NER- 
VOUS SYSTEM. 

(Plates  58  to  72.) 


I.  The  Causes  of  Diseases  of  the  Nervous  System. 

The  diseases  of  the  nervous  system  may  be  either  pri- 
mary aifections  of  the  nerve  substance  itself,  or  secondary 
to  diseases  of  other  tissues  of  the  body,  more  particukirly 
those  in  the  immediate  neighborhood  of  the  brain  (blood- 
vessels, membranes,  bones,  etc.).  The  most  frequent  causes 
of  these  secondary  nervous  diseases  are  : 

(a)  Degeneration  of  the  vascular  apparatus  and  its  con- 
sequences (arteriosclerosis,  thrombosis,  embolism,  rupture, 
aneurysm),  giving  rise  to  various  nutritive  disturbances  or 
to  mechanical  compression  and  destruction  of  the  nerve 
substance. 

(6)  Acute  or  chronic  inflammatory  processes  in  the  cer- 
ebral and  spinal  meninges  (acute  tubercular,  syphilitic 
meningitis,  etc.)  and  in  the  bones  of  the  skull  and  verte- 
bral column  (osteomyelitis,  caries,  gumma).  These  pro- 
cesses may  lead  to  compression  and  nutritive  disturbances, 
or  they  may  spread  by  continuity  to  the  nerve  substance. 

(c)  Tumor  formations  of  every  kind  in  the  tissues  named 
(sarcoma,  carcinoma,  osteoma,  solitary  tubercle,  gumma, 
cysticercus).  These  usually  lead  to  compression  of  the 
adjacent  nerve  substance.  Similar  injuries  may  also  be 
produced  by  cicatrization. 

75 


76     GENERAL  PATHOLOGY  AND  TREATMENT. 

(d)  Metastatic  processes  derived  from  purulent  foci 
(pyemia,  pulmonary  abscess),  tubercular  foci,  or  malignant 
tumors  in  other  organs. 

(e)  Intoxication  in  consequence  of  toxic  materials  being 
taken  up  or  formed  in  the  blood  when  diseased  foci  are 
present  in  other  parts  of  the  body  (diphtheria,  septicemia, 
erysipelas,  typhoid,  syphilis,  nephritis,  diabetes,  etc.). 

(/)  General  constitutional  diseases  (anemia,  cachexia, 
chlorosis,  etc.). 

The  diseases  mentioned  under  (f)  and  (/)  are  frequently 
included  among  the  primary  diseases  of  the  nervous  sys- 
tem. In  addition  this  group  embraces  a  series  of  other 
toxic  and  infectious  diseases  which  manifest  themselves  in 
the  nervous  system  itself :  poisoning  by  lead,  arsenic, 
secale,  and  alcohol ;  acute  poliomyelitis,  acute  myelitis, 
tabes  dorsalis,  acute  neuritis,  etc. 

Here  belong  also  the  diseases  due  to  embryonal  predis- 
position (muscular  atrophy,  hereditary  systemic  diseases, 
etc.)  and  the  group  of  functional  diseases  of  the  nervous 
system. 

Diseases  are  termed  functional  when,  with  our  present 
methods  of  examination,  it  is  impossible  to  demonstrate 
any  anatomic  change  in  the  nervous  system  to  account 
for  them.  In  such  diseases  we  lack,  therefore,  an  exact 
knowledge  of  the  seat  and  character  of  the  disease.  They 
are  considered,  correctly  or  incorrectly,  as  disturbances  in 
the  transmission  of  the  nervous  function  (due  to  molecu- 
lar, chemic  morbid  processes).  As  our  methods  of  exam- 
ination are  perfected  their  domain  is  constantly  dimin- 
ishing. They  include  at  present  hysteria,  neurasthenia, 
genuine  epilepsy,  chorea,  and  a  series  of  psychic  distur- 
bances, such  as  melancholia,  mania,  etc.  In  contradistinc- 
tion to  the  functional  diseases  just  mentioned,  nervous 
diseases  with  demonstrable  anatomic  alterations  are  termed 
organic  and  localizable  diseases. 

Nervous  diseases  are  also  divided  according  to  their 
etiology.     Thus  we  speak  of  endogenous  diseases  when 


CLASSIFICATION  AND  ETIOLOGY.  77 

they  are  due  to  organic  predisposition,  and  of  exogenous 
or  acquired  diseases  (toxic,  infectious,  etc.).  But  in  view 
of  our  imperfect  knowledge  in  regard  to  the  etiology,  and 
especially  for  didactic  reasons,  it  is  advisable  in  the  classi- 
fication to  take  account  of  the  other  principle  as  well. 

In  regard  to  endogenous  diseases  of  the  nervous  sys- 
tem, or  such  as  are  due  to  faulty  embryonal  predisposition, 
it  may  be  said  that  there  is  a  group  of  diseases,  one  or  the 
other  of  which  may  appear  repeatedly,  either  in  the  same 
or  in  a  similar  form,  in  various  members  of  the  same  fam- 
ily. How  the  defect,  whatever  it  may  be,  originally  en- 
tered the  family  we  are  unable  to  explain. 

As  in  the  case  of  most  organs, — heart,  kidney,  liver, — 
the  parenchymatous  material  used  up  in  the  function  of 
the  organ  can  not  be  completely  replaced  in  old  age,  and 
a  senile  atrophy  of  the  organ  must  therefore  result,  espe- 
cially of  its  parenchymatous  elements.  AVe  can  readily 
understand,  therefore,  that  in  many  individuals  this  senile 
exhaustion  of  individual  organs  or  parts  of  organs  may 
occur  prematurely  if  those  individuals  have  not  originally 
been  supplied  with  the  necessary  vital  force.  In  such 
cases  atrophy  of  the  parts  will  take  place  as  soon  as  the 
power  of  replacing  the  used-up  material  is  lost  (cirrhosis 
of  the  liver,  contracted  kidney,  etc.).  The  same  principle 
applies  to  various  nerve  tracts.  Owing  to  some  embry- 
onal defect  the  nerve  tract  is  gradually  destroyed,  often 
many  years  before  the  death  of  the  individual,  and  noth- 
ing will  avail  to  arrest  the  destructive  process  (involution 
diseases). 

Recently  the  theory  has  been  advanced  that  the  choice 
of  the  nerve  tracts  which  degenerate  in  this  way  is  deter- 
mined by  the  character  of  the  function  which  they  sub- 
serve. Moreover,  that  those  tracts  which  are  used  most 
(reflex  tracts,  sensory  tracts,  pyramidal  tracts)  are  most 
liable  to  undergo  this  degeneration,  especially  if  any 
nutritive  disturbances  already  exist  in  other  parts  of  the 


7 8     GENERAL  PA  THOLOG  Y  AND  TREA  TMENT. 

body  (cachexia,  intoxication).     This  theory  appears  to  be 
confirmed  by  some  cases  and  disproved  by  others. 

Even  in  the  exogenous  diseases  of  the  nervous  system, 
congenital  or  acquired,  predisposition,  the  true  nature  of 
which  is  not  well  understood,  undoubtedly  plays  au  im- 
portant role.  In  many  diseases  it  is  possible  to  demon- 
strate one  or  more  concurrent  exciting  causes,  such  as 
undue  mental  exertion,  excesses  of  all  kinds,  and  a  count- 
less variety  of  constitutional  diseases. 


2.  Pathologic  Alterations  in  Nervous  Diseases. 

The  disease  may  affect  arbitrarily  a  certain  portion  of 
the  nervous  system  and  the  nerve-cells  and  nerve-fibers 
which  it  may  happen  to  contain  (diffuse  or  focal  diseases, 
in  the  spinal  cord  :  transverse  myelitis).  Again,  it  may 
be  confined  to  a  combination  of  cells  or  fibers  or  even 
entire  neurons  which  are  anatomically  and  functionally 
related  to  each  other ;  or,  finally,  it  may  involve  an  entire 
pathway  (system  diseases). 

If  two  or  more  different  combinations  of  neurons  or 
tracts  are  attacked  at  the  same  time,  we  speak  of  a  com- 
bined system  disease.  In  focal  diseases,  for  instance, 
the  corresponding  area  of  nervous  substance  is  destroyed 
by  an  extravasation  of  blood.  There  results  from  this  a 
defect  on  the  surface  of  the  organ,  or  a  cavity  within  the 
substance  of  the  organ,  in  which  the  remains  of  the  color- 
ing material  of  the  blood  can  often  be  demonstrated  long 
afterward,  although  the  greater  part  of  the  contents  may 
have  undergone  absorption. 

In  nutritive  disturbances,  such  as  arterial  obstruction, 
compression,  or  inflammatory  processes,  softening  or  sup- 
puration takes  place  if  pyogenic  micro-organisms  are 
present.  The  cells  and  nerve-fibers  involved  undergo 
necrosis  and  degenerate  completely.  The  products  of 
decomposition,  consisting  of  granules  of  fat  and  albumin, 


SECONDARY  DEGENERATIONS.  79 

are  carried  off  by  the  leukocytes  (granule  cells).  In  this 
case  also  a  defect  or  a  cyst  finally  results.  The  neuroglia 
surrounding  a  defect  becomes  greatly  thickened,  and  forms 
an  envelop  which  also  partially  fills  the  cavity  of  the  cyst 
itself.  This  process  of  cicatrization  eventually  results  in 
shrinking  of  the  affected  focus. 

But  in  addition  to  these  inflammatory  consequences 
every  focal  disease  gives  rise  secondarily  to  a  number  of 
other  morbid  processes.  We  have  the  so-called  secon- 
dary degenerations,  both  ascending  and  descending,  vary- 
ing in  the  different  nerve  tracts  and  in  part  extending 
throughout  the  entire  nervous  system.  The  mechanism 
of  these  secondary  degenerations  is  as  follows  : 

Every  neuron  cell,  as  we  have  seen,  exerpises  a  nutri- 
tive influence  on  its  component  parts,  the  processes. 
Destruction  of  the  cell  or  interruption  of  its  connection 
with  the  corresponding  cell-fiber  is  followed  by  secondary 
degeneration  of  the  distal  extremity  of  the  fiber.  The 
neuron  cell  itself  also  suffers  secondary  alterations  if  the 
fiber  is  divided  in  its  continuity  and  the  function  is  thus 
interfered  with.  After  a  solution  of  continuity  has  taken 
place,  the  degenerative  process  begins  immediately  in  that 
part  of  the  neuron  which  is  nearest  the  periphery, — that 
is  to  say,  its  terminal  divisions, — and  eventually  spreads 
to  the  entire  course  of  the  system  affected.  In  other 
words,  the  degenerative  process  in  any  portion  of  a  fiber 
separated  from  its  cell  begins  at  the  periphery  and  works 
toward  the  controlling  cell.  If  the  solution  of  continuity 
is  complete  and  sudden  (trauma),  the  degeneration  takes 
place  in  a  few  weeks  or  months,  and  an  irreparable  gap 
results  at  the  site  of  the  degenerated  nerve  tract.  Regen- 
eration, which  takes  place  only  in  peripheral  nerves,  is 
effected  by  the  proliferation  of  germinal  cells  from  cells 
of  the  sheath  of  Schwann,  which  eventually  succeed  in 
reconstructing  the  nerve-fiber. 

Secondary  degeneration,  or  complete  loss  of  the  fiber, 
is  to  be  distinguished  from  secondary  atrophy  or  simple 


80     GENERAL  PATHOLOGY  AND  TREATMENT. 

diminution  in  the  bulk  of  fibers  and  cells.  It  occurs 
when  the  connection  with  the  primary  focus  is  only  me- 
diate, although  the  normal  function  is  suspended. 

Disease  foci  in  the  cerebral  cortex  give  rise  to  secon- 
dary degeneration  of  the  projection  and  association  fibers 
which  take  their  origin  at  that  point.  In  the  case  of  the 
latter  degeneration  is  usually  only  partial,  because  func- 
tion may  still  be  carried  on  by  means  of  collaterals  which 
may  have  escaped.  Secondary  degeneration  also  occurs 
in  the  optic  thalamus.  Secondary  atrophy  develops  in 
the  various  parts  of  the  subthalamic  region,  the  fillet,  the 
red  nucleus,  and  the  brachium  of  the  opposite  side,  while 
the  remaining  pathways  and  nuclei  escape. 

In  lesions  of  the  mesencephalon  there  is  ascending  and 
descending  degeneration  of  the  fillet  and  degeneration  of 
the  red  nucleus  and  of  the  optic  tract,  while  atrophy  occurs 
in  the  ganglia  of  the  pons,  the  brachia,  the  corpus  denta- 
tum  of  the  cerebellum,  etc.  In  lesions  of  the  cerebellum 
degeneration  takes  place  in  the  restiform  body,  inferior 
olive,  middle  peduncle  of  the  cerebellum,  etc.,  while 
atrophy  takes  place  in  the  red  nucleus  of  the  opposite 
side,  the  brachia,  etc.  Lesions  of  the  spinal  cord  are  fol- 
lowed by  ascending  degeneration  of  the  sensory  pathways, 
especially  the  long  pathways  (columns  of  Goll,  the  cere- 
bellar lateral  tract),  and  descending  degeneration  of  the 
motor  pathways  (pyramids,  anterior  and  lateral  columns 
of  the  cord,  etc.).  (For  further  details  see  Plates  65 
to  72.) 

Some  pathways  appear  to  possess  the  faculty  of  under- 
going degeneration  in  both  directions — as,  for  instance,  the 
tract  of  the  fillet.  These  nerve  paths  probably  contain 
fibers  of  different  origin. 

Under  the  microscope  the  anatomic  alterations  appear 
to  be  practically  the  same  in  primary  as  in  secondary  de- 
generation of  the  nervous  tissue.  But  it  is  to  be  remem- 
bered that,  apart  from  coarse  morphologic  alterations,  w^e 
know  very  little  of  the  more  delicate  morbid  processes  in 


SYMPT03IAT0L0GY  AND  DIAGNOSIS.  81 

the  nerve-cell  and  nerve-fiber.  In  the  ganglion  cells  the 
protoplasm  becomes  cloudy,  then  degenerates,  and  finally 
shrinks.  The  cell  becomes  separated  from  its  processes 
and  the  latter  may  eventually  disappear  entirely,  or  we 
may  have  the  formation  of  vacuoles  and  abnormal  pigmen- 
tation. The  nerve-fibers  swell  up  to  five  or  even  ten  times 
their  normal  size,  the  medullary  sheath  breaks  up  into 
drops  and  finally  undergoes  absorption,  while  the  axis- 
cylinder  may  disappear  either  before  or  after  the  degener- 
ation of  the  sheath  (degenerative  process).  The  spaces  left 
by  the  disappearance  of  the  nerve-cells  and  fibers  become 
filled  with  a  close  network  of  newly  formed  neuroglia  con- 
taining numerous  blood-vessels  with  thickened  walls  ;  fre- 
quently round-celled  infiltration  and  granule  cells  may  be 
seen.  (See  p.  79.)  The  final  stage  is  a  so-called  sclerosis 
or  substitution  of  cicatricial  connective  tissue  for  the  degen- 
erated nerve-fibers.     (See  Plate  63.) 

3.  Symptomatology  and  Topical  Diagnosis  of  Ner- 
vous Diseases. 

The  nervous  tissues  may  react  to  the  various  morbid  pro- 
cesses in  one  of  two  ways  :  either  they  are  stimulated  to  a 
morbid  activity  or  the  function  is  inhibited  and  finally 
abolished  altogether.  Frequently  the  two  phenomena 
merge  into  one  another,  so  that  in  the  beginning  of  the 
disease  the  irritative  symptoms  will  be  more  pronounced, 
and,  as  the  disease  progresses,  the  paretic  phenomena  or 
abolition  of  function  become  more  conspicuous. 

Disease  of  the  motor  corticonmscidar  pathway  may  give 
rise  to  irritative  symptoms  in  the  form  of  general  convul- 
sions, muscular  spasms  (tonic  or  persistent,  and  clonic  or 
intermittent),  coarse  and  fibrillar  muscular  twitchings,  and 
to  paralytic  symptoms  in  the  form  of  weakness  (paresis  or 
paralysis)  of  one  or  more  groups  of  muscles,  depending  on 
the  extent  of  the  diseased  area. 

Disease  of  the  sensory  pathway  may  be  followed  by  irri- 
6 


82     GENERAL  PATHOLOGY  AND  TREATMENT, 

tative  symptoms  in  the  form  of  violent  neuralgic  pains, 
morbidly  increased  sensibility  (hyperesthesia,  hyperalgesia), 
and  by  paralytic  symptoms  in  the  form  of  impairment  or 
complete  loss  of  sensibility  or  only  of  special  kinds  of  sen- 
sation (anesthesia,  analgesia,  thermo-anesthesia).  A  dis- 
ease of  the  pathways  of  coordination  produces  partial  or 
complete  loss  of  coordination  in  muscular  movements 
(ataxia  :  motor  ataxia,  static  ataxia). 

The  character  of  the  symptoms  depends  less  on  the 
nature  of  the  morbid  process  than  on  its  localization  and 
extent.  In  this  connection  it  is  imj)ortant  to  distinguish 
between  focal  and  system  diseases.  In  the  latter  the 
symptoms  are  much  more  constant  and  logical  than  in  the 
former,  in  which,  of  course,  they  vary  according  to  the 
topography  of  the  diseased  focus.  The  interpretation  of 
the  symptoms  of  nervous  diseases  rests  on  the  following 
principles : 

A  lesion  of  the  central  motor  neuron  is  followed  by 
paralysis  of  the  muscles  which  it  supplies,  the  muscular 
action  being  withdrawn  from  the  control  of  the  will  power. 
Since  the  central  neuron  undergoes  decussation,  the  par- 
alysis must  affect  the  opposite  half  of  the  body.  The 
paralysis  is  spastic, — that  is  to  say,  the  affected  muscles 
offer  a  resistance  to  passive  movements, — the  muscular 
tone  is  heightened  (hypertonia),  and  the  muscles  evince  a 
tendency  to  undergo  spontaneous  shortening  (contractures). 
Except  for  a  moderate  degree  of  "  atrophy  from  disuse," 
there  is,  as  a  rule,  no  true  degenerative  muscular  atrophy 
— that  is,  the  amount  of  protoplasm  in  the  muscle  is  not 
diminished.  The  reflex  arc  is  not  interrupted  ;  on  the 
contrary,  the  reflexes  are  heightened.  If  the  lesion  is  in 
the  vicinity  of  the  cells  of  this  neuron  (cortex,  central  con- 
volutions), the  initial  irritative  symptoms  may  consist  in 
involuntary  twitchings  of  the  muscle  or  muscles  affected, 
motor  irritative  symptoms,  tonic  and  clonic  spasms,  epi- 
leptiform convulsions  (on  one  or  both  sides  of  the  body), 
choreic    movements,   or    slow    involuntary   incoordinate 


SYMPTOMATOLOGY  AND  DIAGNOSIS.  83 

movements,  athetosis,  or  involuntary  excessive  and  unus- 
ual movements  of  the  fingers,  etc. 

A  lesion  of  the  peripheral  motor  neuron  is  also  fol- 
lowed by  paralysis  of  the  affected  muscle,  but  as  the  lesion 
is  situated  below  the  decussation  of  the  neuron,  the  par- 
alysis will  be  found  on  the  same  side  of  the  body.  In 
this  case  the  muscle  is  flaccid, — that  is,  there  is  no  resist- 
ance to  passive  movement, — muscular  tone  is  diminished 
(hypotonia,  atonia),  and  there  is  no  tendency  to  contrac- 
tures. The  rapidity  with  which  the  muscle  undergoes 
degenerative  atrophy  depends  on  the  character  of  the  dis- 
ease (the  protoplasm  of  the  muscle-fibers  becomes  cloudy, 
and  then  breaks  up  into  granules  and  is  absorbed).  The 
muscle  is  finally  converted  into  a  fibrous  mass  after  the 
protoplasm  of  the  muscular  fibers  has  completely  disap- 
peared. This  change  can  be  seen  microscopically  in  a 
fresh  section  of  muscle.  The  degenerated  muscle  tissue 
shows  the  atrophied  fibers,  which  have  a  reddish  color, 
while  the  sound  tissue  is  dark  red.  (See  also  Electric 
Diagnosis  in  Part  IV.) 

The  reflex  arc  is  interrupted  and  the  reflexes  are  there- 
fore abolished.  The  fibrillary  muscular  twitchings,  in 
which  only  very  small  fasciculi  of  the  affected  muscles 
participate,  without  producing  any  motion  in  the  muscle, 
are  often  to  be  regarded  as  irritative  symptoms ;  the  mus- 
cle may  be  in  a  condition  of  constant  undulatory  vibra- 
tion until  this  symptom  also  disappears. 

In  lesions  of  the  sensory  pathway  sensation  is  affected 
on  the  opposite  side  of  the  body  in  disease  of  the  central^ 
on  the  same  side  in  disease  of  the  peripheral,  neuron.  The 
differences  in  the  symptoms  are,  however,  not  so  marked 
as  in  lesions  of  the  motor  pathway.  The  irritative  symp- 
toms, consisting  of  violent  neuralgic  attacks  of  pain,  are 
referred  to  the  posterior  roots  (peripheral  neuron). ^ 

Since  the  motor  tract  traverses  the  entire  nervous  sys- 

^  Painful  sensations  are  also  said  to  occur  in  central  disease  or  focal 
disease  in  the  last  third  of  the  posterior  limb  of  the  internal  capsule. 


84     GENERAL  PATHOLOGY  AND  TREATMENT. 

tern,  and  in  its  course  from  the  medulla  downward  the 
central  portion  successively  gives  off  the  peripheral  parts, 
the.  motor  symptoms  observed  in  focal  diseases  affecting 
the  central  pathway  are  utilized,  so  to  speak,  as  the 
abscissa,  while  the  other  focal  symptoms  correspond  with 
the  ordinates  and  thus  indicate  the  level  of  the  lesion. 

We  shall  now  proceed  to  a  description  of  the  symptoms 
of  focal  and  system  diseases. 


I.  SYMPTOMS   OF   FOCAL  DISEASES. 

A.  Cerebral  Diseases. 

These  are  divided  into  direct  or  focal  symptoms  in  the 
true  sense  of  the  term,  and  indirect  or  remote  effects  on 
neighboring  portions  of  the  brain,  and,  finally,  into  general 
symptoms  depending  on  the  nature  and  development  of 
the  lesion.  The  latter  include  fever,  cachexia,  vomiting, 
headache,  and  disturbances  of  the  psychic  activity.  Ex- 
tensive lesions  are  accompanied  by  disturbance  of  con- 
sciousness (coma,  somnolence).  The  following  description 
includes,  of  course,  only  the  direct  focal  symptoms. 

I.  Symptoms  of  Cortical  Lesions. — (a)  Frontal 
Lobe. — A  disease  of  the  frontal  lobe  often  runs  its  course 
without  producing  any  symptoms.  If  the  diseased  focus 
is  very  extensive,  there  may  be  psychic  disturbances 
(apathy,  dementia,  lack  of  concentration).  If  the  poste- 
rior segment  of  the  inferior  frontal  convolution  on  the  left 
side  is  principally  involved,  there  will  be  motor  aphasia. 
If  the  lesion  is  even  more  extensive  and  includes  the  arm 
center  in  the  central  convolutions,  there  may  be  agraphia 
also  (inability  to  write  spontaneously).  In  lesions  of  both 
frontal  lobes,  especially  tumors,  disturbances  of  movement 
of  the  trunk  (consisting  of  a  kind  of  ataxia)  and  of  phona- 
tion  have  been  observed. 

(b)  Central  Convolutions. — Disease  of  the  upper  third 
and  of  the  paracentral  lobule  is  followed  by  spastic  par- 


DISEASE  OF  THE  CENTRAL  CONVOLUTIONS.  85 

alysis  of  the  entire  lower  extremity  of  the  opposite  side — 
crural  monoplegia;  irritative  symptoms,  if  present,  con- 
sist* in  clonic  twitchings  and  choreic  or  athetoid  move- 
ments of  the  leg. 

Lesion  of  the  middle  third  is  followed  by  spastic 
monoplegia  brackialis  of  the  opposite  side,  and  sometimes 
by  irritative  motor  phenomena  in  that  extremity. 

Lesion  of  the  lower  third  gives  rise  to  facial  monoplegia 
of  the  opposite  side,  and  sometimes  to  twitchings  in  this 
portion  of  the  territory  of  the  facial  nerve.  Only  the 
lower  muscles  supplied  by  the  facial  are  involved. 

Lesion  in  the  area  below  and  in  front  of  the  center  for 
the  face  is  followed  by  lingual  monoplegia,  or  paralysis  of 
the  hypoglossus,  on  the  opposite  side ;  the  tongue  is  turned 
toward  the  paralyzed  side. 

If  the  diseased  area  in  the  central  convolutions  is  exten- 
sive and  includes  more  than  one  center,  it  follows,  of 
course,  that  more  groups  of  muscles  on  the  opposite  side 
will  be  involved — partial  or  total  hemiplegia  (with  total 
paralysis  of  the  extremities,  the  facial  and  hypoglossus 
nerves,  and  of  speech).  The  irritative  symptoms  in  cor- 
tical lesions  in  this  area,  especially  when  due  to  trauma, 
consist  in  cortical,  partial,  or  Jacksonian  epilepsy.  They 
are  characterized  by  the  successive  irritation  through  the 
association  bundles  of  all  the  motor  centers  in  the  order  of 
their  position,  beginning  with  the  one  in  the  primary 
focus,  so  that  the  convulsions  occur  in  the  same  order  on 
the  opposite  side  of  the  body  (leg,  arm,  face,  or  in  the 
inverse  order).  Moreover,  they  may  even  be  conveyed  to 
the  other  hemisphere  by  means  of  the  commissural  fibers. 
There  is  also  a  sensory  Jacksonian  epilepsy,  similar  to  the 
motor  variety,  which  manifests  itself  as  an  irritative  con- 
dition in  the  sensory  and  speech  centers. 

In  the  case  of  focal  disease  situated  in  the  central  con- 
volutions of  both  hemispheres  there  will  be  bilateral 
spastic  paralysis,  diplegia  facialis,  brachialis,  etc.  (or  pseu- 
dobulbar paralysis). 


86     GENERAL  PATHOLOGY  AND  TREATMENT. 

The  paralysis  in  these  cases  is  spastic  (see  p.  82).  The 
tendon  reflexes  on  the  paralyzed  side,  and  frequently  on 
the  other  side  as  well,  are  heightened,  while  the  cutaneous 
reflexes  on  the  other  side  are  often  diminished. 

(c)  Parietal  Lobe. — A  lesion  of  this  lobe  is  sometimes 
followed  by  disturbances  of  sensation  in  the  opposite  half 
of  the  body  (muscular  and  cutaneous  sensations)  ;  the 
nature  of  this  disturbance  (hemianesthesia)  is  not  very 
well  understood.  Lesion  in  the  angular  gyrus  may  be 
followed  by  disturbances  in  the  oculomotor  muscles,  such 
as  ptosis  of  the  opposite  eye  and  deviation  of  both  eyeballs 
toward  the  side  of  the  lesion  (conjugate  deviation).  A 
lesion  of  the  inferior  parietal  convolution  (angular  gyrus) 
on  the  left  side  is  said  to  produce  alexia,  or  inability  to 
read,  while  the  power  of  speech  is  not  aifected. 

(d)  Occipital  Lobe. — Destruction  of  one  occipital  lobe 
is  followed  by  the  visual  disturbance  known  as  hemianopsia^ 
or  blindness  of  the  temporal  half  of  one  retina  and  the 
nasal  half  of  the  other,  or  vice  versa.  For  instance,  if  the 
left  lobe  is  destroyed,  there  will  be  blindness  of  the  left 
half  of  each  retina,  or,  in  other  words,  loss  of  vision  in  the 
right  half  of  the  visual  field — right-sided  hemianopsia.  If 
the  lesion  is  more  extensive,  especially  if  situated  in  the 
left  hemisphere,  there  may  be  loss  of  visual  memory  pic- 
tures and  their  associations,  or  psychic  blindness — that  is, 
inability  to  interpret  or  perhaps  only  to  name  an  object 
seen  (visual  aphasia).  If  the  lesion  is  unilateral,  there 
may  be  total  cortical  blindness. 

(e)  Temporal  Lobe. — Destruction  of  the  superior  tem- 
poral convolution  in  the  left  hemisphere  is  followed  by 
loss  of  the  auditory  word-sound  memory  images  and  their 
associations,  or  sensory  aphasia — that  is,  inability  to  un- 
derstand the  m'^anings  of  words,  although  the  power  of 
speech  is  retained. 

In  bilateral  lesions  there  may  be  cortical  deafness  or 
sound-deafness. 

(f)  Mesial  Surface  of  the  Hemispheres. — The  para- 


LESIONS  OF  THE  INTERNAL  CAPSULE.  ^7 

central  lobule  belongs  to  the  central  convolutions  ;  the 
cuneus  to  the  occipital  lobes.  Destruction  of  the  uncinate 
gyrus  (gyrus  hippocampi)  is  said  to  be  followed  by  central 
anosmia,  and  a  lesion  of  the  posterior  basal  segment  of  the 
parietal  lobe,  by  a  central  agemia  ;  the  symptoms  are  pro- 
nounced only  in  bilateral  lesions. 

(g)  The  Insula. — A  lesion  of  the  left  side  of  the  insu- 
lar region  produces  a  disturbance  in  the  associative  activ- 
ity between  the  speech  centers  (probably  because  of  de- 
struction of  the  fasciculus  uncinatus).  There  is  a  partial 
inability  to  form  words  and  sentences — paraphasia,  etc. 
There  is  a  want  of  control  of  the  sensory  speech  center. 

2.  Lesions  of  the  Centrum  Semiovale. — These  often 
produce  no  symptoms  at  all.  If  the  lesion  involves  the 
destruction  of  nerve  paths  heading  from  the  above-men- 
tioned cortical  areas  (subcortical  lesions),  the  same  symp- 
toms may  be  produced  as  in  destruction  of  the  cortex,  ex- 
cept that  there  are  usually  no  irritative  phenomena.  Thus 
there  may  be  monoplegia,  aphasia,  hemianopsia  (optic 
radiation),  and  hemianesthesia.  As  the  central  motor 
pathways  tend  to  converge  as  they  descend  into  the  white 
matter,  a  great  number  of  fibers  are  often  involved  in  a 
comparatively  small  lesion.  Whereas  in  cortical  lesions 
monoplegia  predominates,  total  or  partial  hemiplegia  more 
frequently  results  from  subcortical  lesions. 

Lesions  of  the  corpus  callosum  usually  produce  no 
symptoms, 

3.  Lesions  of  the  Internal  Capsule. — (a)  Destruc- 
tion of  the  anterior  limb  usually  does  not  give  rise  to  any 
demonstrable  symptoms. 

(Jj)  Destruction  of  the  posterior  limb,  if  the  knee  only 
is  involved,  produces  paralysis  of  the  facial  (lower) 
and  of  the  hypoglossus  (if  on  the  left  side,  aphasia)  of 
the  opposite  side.  If  the  lesion  is  bilateral,  diplegia ; 
if  the  central  portion  is  involved,  hemiplegia  of  the  arm 
and  leg  of  the  opposite  side  ;  if  the  seat  of  the  lesion 
is  in  the  posterior  portion,  partial  hemianesthesia  of  the 


88     GENERAL  PATHOLOGY  AND  TREATMENT. 

opposite  side  of  the  body,  hemianopsia,  and  sometimes 
impairment  of  hearing  (?).  As  a  rule,  the  lesion  is  so  ex- 
tensive that  the  greater  part  of  the  internal  capsule  is  de- 
stroyed, and  in  that  case  all  the  phenomena  mentioned  are 
present  together  (total  hemiplegia  of  the  face,  tongue,  arm, 
and  leg  of  the  opposite  side  of  the  body,  with  hemianes- 
thesia, hemianopsia,  etc.). 

The  eye  muscles,  the  muscles  of  mastication,  the  upper 
branches  of  the  facial,  and  the  muscles  of  the  neck  and 
trunk  are  paralyzed  only  in  bilateral  lesions,  as  they  have 
an  independent  innervation  on  both  sides  of  the  body. 

4.  Lesions  of  the  Corpus  Striatum. — Lesions  of  the 
corpus  striatum  do  not  appear  to  be  necessarily  productive 
of  any  symptoms,  and  the  phenomena  that  usually  accom- 
pany them  are  to  be  attributed  to  involvement  of  the  ad- 
jacent inner  capsule  (indirect  symptoms). 

5.  Lesion  of  the  optic  thalamus,  especially  when 
bilateral,  is  followed  by  disturbances  of  the  psychic  re- 
flexes, such  as  laughing,  weeping,  etc. 

In  addition  to  disturbances  of  coordination  choreic  irri- 
tative phenomena  and  muscular  atrophy,  developing  with 
unusual  rapidity  on  the  other  side  of  the  body,  have  been 
referred  to  lesions  in  this  area. 

Destruction  of  the  posterior  section  of  the  optic  thala- 
mus (pulvinar)  is  followed  by  partial  hemianopsia. 

6.  Lesions  in  the  subthalamic  region  are  followed  by 
crossed  hemianesthesia  (lesion  of  the  fillet). 

7.  Lesions  of  the  Corpora  Quadrigemina.  —  The 
symptom  produced  is  a  peculiar  disturbance  of  the  gait — 
stumbling,  uncertain  gait,  cerebellar  ataxia,  explained 
either  by  participation  of  the  brachium  or  by  remote 
effects  on  the  adjoining  cerebellum  (?).  This  peculiar 
gait,  however,  can  be  utilized  as  a  sign  of  disease  in  the 
corpora  quadrigemina  only  when  it  is  combined  with  other 
symptoms,  as,  for  instance,  ophthalmoplegia.  This  form 
of  paralysis  may  be  nuclear,  or  due  to  lesion  in  the  oculo- 
motor Jibers,  and  may  be  either  unilateral  or  bilateral,  ac- 


LESIONS  OF  CORPORA  QUADRIGEMINA  AND  PONS.     89 

cording  to  the  situation  ;  bilateral  especially  in  the  nuclear 
form  (probably  on  account  of  the  close  proximity  of  the 
nuclei).  Lesions  in  the  more  anterior  nuclei  situated  in 
the  lateral  wall  of  the  third  ventricle  appear  to  produce 
paralysis  of  the  internal  muscles  of  the  eye  (the  ciliary 
muscles,  spliincter  pupillse).  If  the  lesion  is  situated 
beneath  the  anterior  corpora  quadrigemina,  paralysis  of 
the  internal  rectus,  superior  rectus,  and  levator  palpe- 
brarum superior  is  produced.  The  other  nuclei  of  the 
ocular  muscles  are  situated  more  posteriorly.  The  abdu- 
cens  escapes.  If  the  lesion  involves  the  tegmentum  under 
the  corpora  quadrigemina  (fillet),  there  will  be  incomplete 
hemianesthesia  of  the  opposite  side.  Injury  to  the  crusta 
produces  hemiplegia  of  the  arm  and  leg  on  the  opposite 
side,  and  sometimes  facial  and  lingual  hemiplegia. 

If  the  lesion  is  unilateral,  there  will  be  total  hemiplegia 
of  the  opposite  side,  with  oculomotor  paralysis  of  the  same 
side  (peripheral  neuron  of  the  same  side).  This  form  of 
hemiplegia  in  which,  in  addition  to  the  decussating  central 
neurons,  certain  uncrossed  peripheral  neurons  are  involved 
in  the  lesion,  is  known  as  hemiplegia  alternans  (crossed 
hemiplegia).  If  the  lesion  is  bilateral,  the  symptoms  are 
modified  in  accordance  with  the  extent  of  the  lesion. 

The  paralyzed  eye  muscles,  of  course,  undergo  degen- 
erative atrophy,  while  the  paralysis  in  the  extremities  is 
spastic  in  character  and  is  not  accompanied  by  any  marked 
degeneration  of  the  muscle  tissue.  If  the  optic  tract  or 
the  lateral  geniculate  body  is  involved  in  the  lesion,  there 
is  total  or  partial  hemianopsia.  In  destruction  of  the  pos- 
terior corpus  quadrigeminum  and  the  median  geniculate 
body  the  hearing  is  often  disturbed,  especially  if  the  lesion 
is  bilateral. 

8.  Lesions  of  the  Pons. — Unilateral  lesions  may  be 
followed  by  hemianesthesia  (fillet),  brachiocrural  hemi- 
plegia (pyramidal  tract  of  the  opposite  side  of  the  body) ; 
paralysis  of  the  muscles  of  mastication  on  the  same  side 
(motor  portion  of  trigeminus,  peripheral  neuron)  or  more 


90     GENERAL  PATHOLOGY  AND  TREATMENT. 

posteriorly  of  the  facial  muscles  of  the  same  side  (periph- 
eral neuron,  hemiplegia  alternans).  Destruction  of  the 
nucleus  of  the  abducens  is  followed  by  combined  oculo- 
motor paralysis  (rectus  externus  of  the  same,  and  rectus 
internus  of  the  opposite,  side).  The  sensory  symptoms 
will  be  anesthesia  in  the  region  of  the  trigeminus  of  the 
same  side,  disturbances  in  the  sense  of  taste,  disturbances 
in  the  power  of  articulation  (partial  inability  to  form 
letters)  on  account  of  involvement  of  fibers  from  the 
facial  and  hypoglossus.  Irritative  symptoms  in  the  form 
of  vertigo,  ataxia,  and  trismus  may  be  present.  Bilateral 
lesions  produce  corresponding  symptoms. 

9.  Lesions  of  the  Medulla  Oblongata. — If  the  lesion 
is  unilateral,  there  may  be  brachiocrural  hemiplegia  and 
hemianesthesia  of  the  opposite  side  of  the  body.  If  the 
internal  arcuate  fibers  in  the  posterior  segment  of  the 
medulla  are  involved,  there  may  even  be  bilateral  hemi- 
anesthesia (the  lesion  is  situated  below  the  decussation  of 
the  fillet).  In  addition  there  may  be  paralysis  of  the 
hypoglossus  of  the  same  side  (peripheral  neuron,  hemi- 
plegia alternans). 

The  tongue  is  turned  to  the  side  of  the  lesion ;  the 
muscles  on  the  corresponding  side  are  degenerated.  As  a 
result,  there  will  be  defective  articulation  or  bulbar  speech, 
unaccompanied  by  disturbance  of  the  speech  center  (dys- 
arthria labiolingualis). 

Among  other  symptoms  may  be  mentioned  paralysis  of 
the  muscles  of  deglutition,  paralysis  of  the  epiglottis  (fail- 
ure of  the  cartilage  to  close  the  larynx),  dyspnea,  aphonia 
(paralysis  of  the  vocal  cords),  and  circulatory  disturbances, 
especially  if  the  lesion  is  bilateral.  Destruction  of  the 
inferior  olives  is  said  to  be  followed  by  disturbance  of  the 
equilibrium. 

10.  Lesions  of  the  Cerebellum. — The  symptoms  pro- 
duced are  susceptible  of  many  interpretations  and  are  very 
indefinite.  Disease  of  the  vermiform  process  gives  rise  to 
disturbances  of  the  equilibrium,  attacks  of  vertigo,  cere- 


BASAL  LESIONS.  91 

bellar  gait  (tottering  gait),  vomiting,  and  sometimes  occip- 
ital headache. 

A  lesion  in  the  middle  cerebral  peduncle  is  also  followed 
by  disturbance  of  the  equilibrium,  vertigo,  and  forced 
movements  (rotation  about  the  longitudinal  axis). 

Lesions  of  the  hemispheres  may  be  unproductive  of 
symptoms. 

II.  Focal  Diseases  at  the  Base  of  the  Brain. — They 
are  characterized  chiefly  by  simultaneous  paralysis  of  sev- 
eral cranial  nerves,  either  of  the  same  or  of  both  sides 
(oculomotor,  abducens,  facial,  trigeminus,  hypoolossus,etc.). 

A  lesion  may  at  the  same  time  involve  the  crusta 
(hemiplegia  of  the  opposite  side),  the  optic  tract,  and  the 
chiasm. 

It  follows  that  there  may  be  a  great  variety  of  symp- 
toms, and  their  interpretation  should  not  be  difficult. 
(For  further  details  sec  under  Peripheral  Nerves  in  this 
chapter.)  The  most  frequent  associations  are  the  second 
and  third,  the  sixth  and  seventh,  and  the  tenth,  twelfth, 
and  eleventh  (inferior,  middle,  and  posterior  fossse  of  the 
skull). 

To  review  briefly,  a  typical  cerebral  paralysis  consists  of 
spastic  hemiplegia  and  hemianesthesia  of  the  opposite  side. 

In  cortical  lesions  monoplegia  predominates ;  in  lesions 
of  the  capsule,  simple  hemiplegia  ;  in  lesions  of  the  corpora 
quadrigemina  and  crusta,  hemiplegia  with  crossed  oculo- 
motor paralysis  (hemiplegia  alternans  superior). 

In  lesions  of  the  pons,  hemiplegia  with  paralysis  of  the 
trigeminus  and  facial  of  the  opposite  side  (hemiplegia 
alternans  media). 

In  lesions  of  the  medulla  oblongata,  hemiplegia  with 
lesion  of  the  hypoglossus,  etc.,  of  the  opposite  side  (hemi- 
plegia alternans  inferior).  This  is,  of  course,  on  the  sup- 
position that  the  lesion  is  unilateral.  As  the  projection 
fibers  gradually  approach  each  other  more  and  more  in 
their  downward  course  to  the  cord,  there  is  a  correspond- 


92     GENERAL  PATHOLOGY  AND  TREATMENT. 

ingly  greater  possibility  of  the  lesion  producing  bilateral 
symptoms.  This  is  even  more  the  case  in  focal  diseases  of 
the  spinal  cord. 

B.   Focal    Symptoms  in    Lesions  of   the  Spinal  Cord. 

As  hemiplegia  is  the  typical  cerebral  lesion,  so  para- 
plegia, or  paralysis  of  the  extremities,  not  only  of  one,  but 
of  both  sides,  is  the  typical  lesion  of  disease  of  the  spinal 
cord.  This  is  due  to  the  fact  that  the  motor  paths  for 
both  sides  of  the  body  are  situated  comparatively  near 
each  other  in  the  spinal  cord,  and  are,  therefore,  very  apt 
to  be  affected  by  the  same  lesion. 

Unilateral  injuries  of  the  spinal  cord  may,  however, 
occur  from  stab  wounds  or  compression  by  a  tumor,  and 
present  a  very  typical  symptom-complex,  known  as  Brown- 
Sequard's  paralysis,  which  differs  from  tlie  clinical  picture 
seen  in  other  diseases  of  the  spinal  cord. 

Thus  a  unilateral  lesion  of  the  spinal  cord  is  followed 
by  paralysis  of  the  extremities  on  the  same  side,  varying 
more  or  less  according  to  the  seat  of  the  lesion,  while  sen- 
sory disturbances  are  produced  chiefly  on  the  opposite  side 
of  the  body.  This  distribution  follows  naturally  from  the 
fact  that  the  motor  paths  decussate  above  the  beginning  of 
the  spinal  cord  in  the  decussation  of  the  pyramids,  while 
the  sensory  paths  enter  the  spinal  cord  for  the  most  part 
uncrossed  (anterolateral  column,  anterior  commissure). 
There  is,  besides,  a  narrow  zone  of  anesthesia  on  the  par- 
alyzed side,  corresponding  to  the  level  of  the  lesion.  This 
condition  is  due  to  injury  of  the  uncrossed  peripheral  neu- 
rons of  the  same  side  at  their  entrance  into  the  cord. 
Above  this  zone  of  anesthesia  there  is  a  narrow,  girdle-like 
zone  of  hyperesthesia,  due  to  irritation.  The  symptoms 
in  a  lesion  of  one  half  of  the  spinal  cord  are,  however, 
not  always  so  clearly  marked  as  we  have  just  described 
them.  The  following  are  the  more  important  focal  symp- 
toms usually  observed. 


LESIONS  IN  THE  CERVICAL  ENLARGEMENT.  93 

(a)  Lesions  in  the  Cervical  Enlargement. — If  the 
entire  transverse  section  of  the  cord  be  involved,  complete 
paralysis  of  both  arms  and  legs — jjaraplegia  universalis 
— with  complete  anesthesia  of  the  trunk  and  extremities, 
results.  The  paralysis  of  the  legs  is  spastic  (central  neuron), 
that  of  the  arms  flaccid,  if  the  lesion  is  situated  some- 
where between  the  fifth  cervical  and  first  thoracic  vertebrae 
(peripheral  neuron,  anterior  horn).  Those  muscles  of  the 
upper  extremity  whose  trophic  centers  in  the  anterior  horn 
have  been  destroyed  undergo  a  degenerative  atrophy.  The 
tendon  reflexes  in  the  upper  extremities  are  abolished  (in- 
terruption of  reflex  arc),  while  those  in  the  lower  extrem- 
ities are  heightened  (degeneration  of  the  central  inhibitory 
fibers).^  Sensation  is  disturbed  as  high  up  as  the  points 
of  entrance  of  the  posterior  root-fibers  into  the  diseased 
segments.  There  is  also  loss  of  sphincter  control  in  the 
bladder  and  rectum,  on  account  of  the  interruption  in  the 
central  pathways  of  these  organs.  The  intensity  of  the 
symptoms  depends  on  the  extent  of  the  lesion. 

The  flaccid  paralysis  of  the  upper  extremities  affects 
either  all  or  only  certain  groups  of  muscles,  according  to 
the  seat  of  the  lesion.  (For  further  elucidation  on  this 
point  see  Fig.  17  on  p.  52.)  The  most  important  segments 
of  the  cervical  cord  are  the  following : 

a.  Fourth  segment :  Paralysis  of  the  diaphragm. 

ft.  Fifth  and  sixth  segments  :  Paralysis  of  the  upper  arm 
(deltoid,  biceps,  brachialis  anticus,  supinator  longus)  and 
possibly  paralysis  of  the  muscles  about  the  shoulder. 

;'.  Seventh  and  eighth  segments  :  Paralysis  of  the  fore- 
arm (muscles  of  the  forearm,  triceps). 

8,  Eighth  cervical,   first  thoracic  segments  :   Paralysis 

^  About  ten  cases  have  been  reported  in  which  complete  division  of 
the  cord  in  the  cervical  region  was  followed  by  loss  of  the  patellar  reflex. 
Various  explanations  have  been  given  for  these  exceptional  cases, — de- 
generations in  the  lower  reflex  arc,  interferenpe  with  the  reflexes  by- 
shock,  or,  according  to  others,  degeneration  of  the  cerebellar  tracts  to 
the  reflex  center, — but  at  all  events  the  observations  are  not  sufiiciently 
numerous  to  affect  the  truth  of  the  above  statement  in  ordinary  cases. 


94     GENERAL  PATHOLOGY  AND  TREATMENT. 

of  the  small  muscles  of  the  hand  and  occasionally  pupil- 
lary symptoms.  (See  under  C,  1.)  In  all  these  cases  the 
muscles  undergo  degenerative  atrophy. 

(b)  Lesions  in  the  Thoracic  Region. — The  upper  ex- 
tremities are  not  affected  unless  the  first  thoracic  segment 
is  involved  (small  muscles  of  the  hand). 

The  lower  extremities  are  the  seat  of  a  spastic  paralysis 
— paraplegia  inferioi- — with  heightened  reflexes  (patellar 
reflex  and  ankle-clonus,  etc.).  There  is  complete  anesthesia 
(analgesia,  thermotactile  anesthesia,  loss  of  muscular  sense, 
etc.),  extending  to  that  region  of  the  trunk  the  sensory 
fibers  of  which  enter  the  posterior  roots  at  the  level  of  the 
spinal  lesion. 

There  is  also  loss  of  control  of  the  bladder  and  rectum. 
Those  muscles  of  the  trunk  whose  special  segments  are 
included  in  the  lesion  undergo  degenerative  atrophy,  which, 
however,  is  usually  very  difficult  to  demonstrate  (inter- 
costal, lumbar,  dorsal,  abdominal  muscles,  etc.).  (See  Elec- 
tric Diagnosis,  p.  109.)  If  the  paraplegia  persists  for  a 
great  length  of  time,  the  patellar  reflexes  may  become  faint, 
probably  in  consequence  of  the  formation  of  contractures. 

(c)  Lesions  in  the  Lumbar  Enlargement. — Motion 
and  sensation  are  aflected  in  the  lower  extremities  only. 
There  is  a  flaccid  infernor  paraplegia  (peripheral  neuron), 
with  complete  anesthesia,  the  muscles  of  the  legs  under- 
going degenerative  atrophy  and  the  reflexes  being  abol- 
ished. Also  total  paralysis  of  the  bladder  and  rectum 
(sphincter  reflex  preserved,  see  p.  123). 

If  the  lesion  is  situated  in  the  upper  portion  of  the 
lumbar  enlargement,  the  muscles  supplied  by  the  crural 
nerves  (quadriceps,  psoas)  degenerate ;  if  in  the  lower 
portion,  those  supplied  by  the  sciatic  (glutei,  peronei,  mus- 
cles of  the  calf).  (For  more  detailed  information  on  the 
distribution  of  the  paralysis  see  Fig.  17,  p.  52.) 

(d)  Lesions  in  ^le  Sacral  Region. — The  thigh  in  this 
case  escapes,  while  some  of  the  small  muscles  of  the  foot 
become  paralyzed  and  atrophy.     There  is  anesthesia  in 


LESIONS  IN  THE  CAUDA  EQUINA.  95 

the  outer  border  and  toes  of  the  foot  and  in  the  region  of 
the  anus.  There  are  total  vesical  and  rectal  paralysis  and 
loss  of  sphincter  reflexes.  The  patellar  reflex  is  preserved 
because  the  lesion  is  situated  lower  than  the  reflex  arc. 

(e)  Lesions  in  the  Cauda  Equina. — The  symptoms 
are,  in  the  main,  those  of  a  lesion  in  the  lumbosacral  en- 
largement, as  the  Cauda  contains  all  the  nerve  tracts  which 
begin  at  that  point.  If  those  fibers  of  the  crural  nerves 
that  are  the  highest  in  situation  escape,  the  paralysis  will 
appear  chiefly  in  the  muscles  supplied  by  the  sciatic  nerves 
— that  is  to  say,  there  will  be  a  flaccid  paralysis  of  the 
peronei  and  other  muscles  of  the  leg  and  of  the  small 
muscles  of  tlie  foot  (sometimes  also  of  the  flexors  of  the 
thigh  and  of  the  glutei).  Sensation  is  disturbed  in  the 
region  supplied  by  the  sciatic  and  sacral  nerves.  There  is 
complete  paralysis  of  the  bladder  and  rectum  if  the  nerves 
of  these  organs  are  involved.  The  patellar  reflex  will  be 
preserved  if  the  roots  of  the  crural  nerves  are  unaffected, 
otherwise  it  will  be  abolished.  The  Achilles  tendon  reflex 
and  the  sphincter  reflex  are  abolished. 

If  the  posterior  roots  at  the  corresponding  levels  are 
involved  in  the  spinal  lesion,  violent  neuralgic  pains  will 
appear  in  the  region  of  their  distribution ;  sometimes  these 
pains  correspond  only  to  the  highest  roots  affected  by  the 
disease.  Not  infrequently  reflex  muscular  twitchings  in 
the  paralyzed  limbs  are  observed  in  such  cases. 

C.  Symptoms  Observed  in  Lesions  of  the  Peripheral 

Nerves. 

Lesions  of  the  peripheral  nerves  are  followed  by  motor 
and  sensory  disturbances  which  correspond  exactly  to  the 
region  of  their  distribution ;  hence  a  knowledge  of  these 
svmptoms  is  indispensable  for  an  exact  diagnosis.  (See 
Plate  27.) 

The  paralysis  is  flaccid  in  character,  and  the  muscle 
undergoes  degenerative  atrophy  if  the  lesion   is   severe 


96  GENERAL  PATHOLOGY  AND  TREATMENT. 

(peripheral  neuron).  The  sensory  disturbances  are  strictly 
confined  to  the  distribution  of  the  cutaneous  nerve  (in  long- 
standing conditions  the  boundaries  tend  to  become  indis- 
tinct). Painful  and  abnormal  sensations  are  often  com- 
plained of  (paresthesia,  formication,  pricking  sensations, 
furry  feeling,  burning,  etc.).  The  reflexes  are  diminished 
or  lost  if  their  corresponding  arcs  are  included  in  the 
damaged  nerves. 

I.  Plexus  Paralyses. —  The  symptoms  of  plexus 
paralyses  are  made  up  of  a  mixture  of  the  paralytic 
symptoms  of  all  the  nerves  which  compose  them ;  the 
clinical  picture,  therefore,  presents  many  variations.  Some 
of  the  most  typical  and  frequent  lesions  are  the  following  : 

(a)  Erb's  Paralysis  of  the  Brachial  Plexus. — This 
involves  the  fifth  and  sixth  cervical  roots,  destruction  of 
which  is  followed  by  paralysis  and  atrophy  of  the  deltoid, 
biceps,  brachialis  anticus,  supinator  longus,  supra-  and  in- 
fraspinatus. Accordingly,  there  is  inability  to  raise  and 
abduct  the  arm  or  to  flex  the  forearm. 

(b)  Paralysis  of  the  Lower  Portion  of  the  Brachial 
Plexus. — This  involves  the  eighth  cervical  and  first  tho- 
racic roots,  and  leads  to  paralysis  and  atrophy  of  the  small 
muscles  of  the  hand  and  anesthesia  in  the  ulnar  region. 
In  addition  there  may  be,  if  the  first  dorsal  segment  is 
involved,  oculopupillary  symptoms,  as  miosis,  diminution 
in  the  palpebral  fissure,  retraction  of  the  bulb.  The  lower 
extremities  are  not  involved,  the  paralysis  differing  in  this 
respect  from  that  observed  in  lesions  of  the  corresponding 
segments  of  the  spinal  cord. 

II.  Lesions  of  the  Cranial  Nerves. — The  distribu- 
tion of  the  sensory  disturbance  for  the  various  nerve 
trunks  is  shown  in  Figures  23  to  25.  The  symptoms  in 
lesions  of  the  individual  nerves  are  the  following : 

1.  Olfactory  Nerve. — ^Anosmia  of  the  corresponding 
half  of  the  nose  and  parosmia  (disagreeable  odors). 

2.  Optic  Nerve. — Amaurosis  of  the  corresponding  eye 
and  of  the  entire  visual  field,  differing  in  this  respect  from 


LESIONS  OF  THE  CRANIAL  NERVES. 


97 


disease  of  the  optic  tract,  in  which  there  is  hemianopsia,  or 
loss  of  vision  in  one  half  of  the  field.  In  some  cases  there 
is  only  impairment  of  the  visual  acuity — contraction  of 
the  visual  field  and  atrophy  of  the  optic  nerve  (white  pap- 
illa), mydriasis,  and  reflex  pupillary  rigidity,  while  sensual 
reaction  is  preserved. 

In  lesions  of  the  chiasm 
there  is  bitemporal  hem- 
ianopsia (destruction  of 
the  internal  retina  bun- 
dles which  decussate  at 
this  point). 

3.  Oculomotor  Nerve. 
— Ptosis  (paralysis  of  the 
levator  palpebrse  superi- 
oris)  ;  inability  to  rotate 
the  eye  inward  and  up- 
ward (internal  rectus ; 
superior  and  inferior  ob- 
lique); crossed  diplopia ; 
fixation  of  the  bulb  in 
downward  and  outward 
rotation,  owing  to  con- 
tracture of  the  intact  ex- 
ternal rectus.  Further, 
there  are  pupillary  rigid- 
ity and  dilatation(mydri- 
asis),  due  to  interference 
with  the  action  of  the 
sphincter  muscle,  and 
loss  of  accommodation 
for  near  objects  on  ac- 
count of  paralysis  of  the 


) '  \l'. 

'^L 

N 

-A 

A-fe--x/| 

'    % 

r^KL  '   ' 

^ 

/'-^3^  "l  ^'3 

'*\S 

xmm 

/<■  /    If     ; 

^^biflL 

g— 

^ 

W^'^r^. 

«^.; 

''/"' 

SUr/wd. 

-^            \m].'^-*^^ 

h 

1  / 

V-- 

.Y? access pr: 

^h,jp^;^tr^r>. 

li' 

/ 

I 

Ji'ptirenic—^ 

■'xT 

rp 

V 

PUx.bruch. -- 

\ 

\FtuM:Erb^        , 

_'^.- 

\ 

/c- 

'" 

Fig.  23. — Fj,  First  division  of  tri- 
facial: so^  Supra-orbital ;  s^,  supratroch- 
lear; it^  infratrochlear;  e^  ethmoidal; 
laterally,  the  lacrimal.  Fg,  Second 
division  of  trifacial:  ?/,  Infra-orbital; 
labial,  sup.  F^,  Third  division  of  tri- 
facial: ai^  Auriculotemporal;  lab.  inf. ; 
w,  mental,  am,  Auricularis  magnus; 
mai^  occipitalis  minor;  oma^  occipitalis 
major;  cs,  subcutaneus  colli  sup., 
med.,  inf.  (cervical,  ant.);  rp^  cervical, 
dorsal.  The  dots  indicate  where  the 
electric  current  should  be  applied  to 
the  facial,  phrenic,  brachial  plexus,  etc. 


ciliary  muscle. 

4.  Trochlear  Nerve. — Diplopia  in  looking  downward 
(superior  oblique). 

5.  Trifacial   Nerve. — (a)  Supra-orbital  Branch — An- 

7 


98 


GENERAL  PATHOLOGY  AND  TREATMENT. 


estbesia  in  the  skin  of  the  brow  and  bridge  of  the  nose  and 
of  the  conjunctiva.     (See  Fig.  23,  F^.) 

(6)  Infra-orbital  Branch. — Anesthesia  of  the  skin  on  the 
cheeks  and  alse  of  the  nose,  anesthesia  of  the  palate  and 
disturbance  of  the  sense  of  taste  (Fig.  23,  V^). 

(c)  Inferior  MaxiUary  Division. — Anesthesia  of  the  skin 
over  the  lower  jaw  and  of  the  mucous  membrane  of  the 


£xtens  poll. 


Fig.  24. — »i,  Median;  w,  ulnar;  r,  radial;  rp,  posterior  root;  m,  ilio- 
inguinal; sp.e,  external  spermatic. 


tongue  and  mouth  (Fig.  23,  Fg).  Disturbance  of  the 
sense  of  taste  in  the  anterior  segment  of  the  tongue ; 
paralysis  of  the  muscles  of  mastication  and  disturbance  in 
salivary  secretion  ;  trismus  (spasm  of  the  muscles  of  mas- 
tication due  to  irritation).  Irritation  of  the  sensory 
branches  gives  rise  to  trifacial  neuralgia  of  greater  or  less 


LESIONS  OF  THE  CRANIAL  NERVES.  99 

extent,  according  to  the  seat  of  the  lesion  ;  paresthesia  also 
occurs. 

6.  Abducens  Nerve. — Inability  to  rotate  the  eye  out- 
ward (external  rectus) ;  deviation  of  the  bulb  inward,  and 
diplopia  on  the  same  side  when  the  glance  is  directed 
downward. 

7.  Facial  Nerve. — Paralysis  of  the  facial  muscles  of 
expression  (upper  and  lower  facial),  of  the  mouth,  the 
nose,  the  orbicularis  oculi,  and  of  the  forehead.  The  lines 
of  the  face  are  obliterated  ;  the  palpebral  fissure  can  not 
be  closed  (lagophthalmus)  ;  puckering  of  the  lips,  as  in 
whistling,  impossible  ;  inability  to  retract  the  angles  of  the 
mouth,  as  in  laughing. 

Paralysis  of  the  digastric  (posterior  belly),  stylohyoid, 
etc.,  does  not  produce  any  symptoms. 

If  the  lesion  is  situated  Avithin  the  Fallopian  canal,  the 
chorda  tympani  from  the  second  (third?)  branch  of  the 
trifacial  may  be  involved  and  the  sense  of  taste  may  be 
disturbed  in  the  anterior  segment  of  the  tongue. 

The  irritative  symptoms  are :  Convulsions  of  the  mus- 
cles named,  convulsion  of  the  facial  nerve,  or  tic  convulsif, 
and  blepharospasm.  These  symptoms  may,  however,  be 
due  to  reflex  or  central  irritation. 

8.  Auditory  Nerve. — (a)  Cochlear  Nerve. — Deafness, 
paresthesia. 

(b)  Vestibular  Nerve. — Disturbance  of  the  equilibrium  ; 
attacks  of  vertigo  and  vomiting,  with  tinnitus  aurium  and 
whistling  noises — Meniere's  symptom-complex,  especially 
in  hemorrhage  in  the  labyrintli. 

9.  Glossopharyngeal  Nerve. — Partial  disturbance  of 
the  sense  of  taste  (posterior  segment  of  the  tongue) ;  anes- 
thesia of  the  nasopharynx. 

10.  Pneumogastric  Nerve. — (a)  Seyisory  Branch  (True 
Vagus). — Anesthesia  of  the  pharynx,  larynx,  esophagus, 
trachea,  and  bronchi. 

(b)  Motor  Branch  (in  part  derived  from  the  Spinal 
Accessory). — Dysphagia  (paralysis  of  the  esophagus) ;  dis- 


100    GENERAL  PATHOLOGY  AND  TREATMENT. 

turbauces  of  the  gastric,  cardiac,  and  respiratory  functions. 
Paralysis  of  the  recurrent  (paralysis  of  the  vocal  cords) ; 
if  bilateral,  aphonia. 

1 1.  Spinal  Accessory  Nerve. — (a) Pneumogastrie  Branch 
(^Inferior  Laryngeal ). — Paralysis  of  the  recurrent,  as  above. 
Paralysis  of  the  muscles  of  the  palate  and  pharynx. 

(6)  External  Branch. — Paralysis  of  the  sternocleido- 
mastoid and  in  part  of  the  trapezius  (difficulty  in  turning 
the  head  and  raising  the  shoulder) ;  irritative  symptom, 
spasm  of  the  spinal  accessory  or  spastic  torticollis  (wry- 
neck). 

12.  Hypoglossus. — Paralysis  of  one  side  of  the  tongue 
(when  the  tongue  is  protruded,  it  turns  toward  the  para- 
lyzed side),  disturbances  of  the  articulation  (difficulty  in 
forming  the  various  letters). 

III.  Lesions  of  the  more  important  Spinal  Nerves. 
— For  details,  which  can  not  be  given  here,  see  Plate 
27  and  text.  The  distribution  of  the  anesthesia,  which 
is  not  mentioned  here,  will  be  found  in  Figures  24  and  25. 

1.  Great  Occipital  Nerve. — Occipital  neuralgia,  anes- 
thesia.    (See  Fig.  23.) 

2.  Phrenic  Nerve. — Paralysis  of  the  diaphragm  ;  irri- 
tative symptoms,  spasm  of  the  diaphragm,  singultus. 

3.  Axillary  Nerve. — Paralysis  of  the  deltoid  (difficulty 
in  raising  and  abducting  the  arm),  anesthesia.  (See  Fig. 
24.) 

4.  Posterior  Thoracic  Nerve. — Paralysis  of  the  serra- 
tus  magnus  (the  scapula  projects  from  the  thorax ;  inabil- 
ity to  raise  the  arm  beyond  the  horizontal). 

5.  Anterior  Thoracic  Nerves. — Paralysis  of  the  pec- 
toralis  major,  inability  to  abduct  the  arm. 

6.  Musculocutaneous  Nerve. — Paralysis  of  the  biceps 
and  brachial  is  anticus  (flexors  of  the  forearm) ;  anesthesia 
(see  Fig.  24,  lateral  cutaneous  nerve). 

7.  Radial  Nerve. — Paralysis  of  the  triceps  (extension 
of  the  forearm) ;  anconeus  (absence  of  prominence  of  the 
anconeus  in  flexion    of  the  forearm) ;    paralysis    of  the 


LESIONS  OF  THE  SPINAL  NERVES  101 

extensors  of  the  hand,  of  the  first  phalanges  of  the 
fingers,  and  of  the  extensors  and  abductors  of  the  thumb. 
(For  anesthesia  see  Fig.  24,  N.  cut.  post.  sup.  and  m/,  ram, 
dorsalis.)  The  hand  and  fingers  are  paralyzed  and  limp 
(wrist-drop),  and  the  grip  is  considerably  weakened  on 
account  of  paralysis  of  the  antagonistic  muscles. 

8.  Median  Nerve. — Paralysis  of  the  pronator  muscles 
when  the  forearm  is  flexed,  and  of  the  radial  flexors  of 
the  hand,  distal  phahuiges  of  the  fingers,  and  of  the  thumb 
(including  the  flexor  carpi  nlnaris  and  the  ulnar  portion 
of  the  flexor  digitorum  profundus).  Inability  to  adduct 
the  thumb  and  to  extend  the  distal  phalanges  of  the  sec- 
ond, third,  and,  rarely,  of  the  fourth  fingers  (lumbricales). 
(Anesthesia  of  the  integument  supplied  by  the  volar 
branch  of  the  median  nerve,  see  Fig.  24,  m.) 

9.  Ulnar  Nerve. — Paralysis  of  the  flexor  carpi  ulnaris 
and  of  the  ulnar  portion  of  the  flexor  digitorum  profundus 
(distal  phalanges  of  the  fourth  and  fifth  fingers)  ;  inability 
to  flex  the  first  phalanges  (interossei)  or  to  extend  the  dis- 
tal phalanges  of  the  fourth  and  fifth  fingers  (lumbricales). 
Inability  to  adduct  the  thumb  and  flex  its  first  phalanx. 
Owing  to  the  unopposed  action  of  the  antagonistic  mus- 
cles, the  so-called  claw-hand  {main  en  griffe)  is  produced. 
(Anesthesia,  see  Fig.  24,  uln.  superfic  and  dorsalis.) 

In  paralysis  of  the  ulnar,  median,  and  radial  nerves  the 
power  of  writing  is  much  impaired,  and  the  patient  finds 
it  impossible  to  seize  and  hold  things.  Complete  paralysis 
of  even  one  of  these  nerves  materially  affects  the  useful- 
ness of  the  hand. 

10.  Intercostal  Nerves. — Sensory  irritative  symptom, 
intercostal  herpes  zoster.     Anesthesia. 

11.  Crural  Nerve. — Paralysis  of  the  psoas  (elevator  of 
the  thigh)  and  the  quadriceps  (extensor  of  the  leg) ;  ina- 
bility to  walk  or  to  assume  a  standing  posture.  Patellar 
reflex  abolished.  (For  anesthesia  see  Fig.  25,  cruralis, 
middle  and  infernal  femoral  cutaneous,  and  saphenous 
nerve.) 


102 


GENERAL  PATHOLOGY  AND  TREATMENT. 


12.  Obturator  Nerve. — Paralysis  of  the  adductor  mus- 
cles of  the  thigh.     (Auesthesia,  see  Fig.  25.) 

13.  Sciatic  Nerve. — Paralysis  of  the  foot  aud  toes  and 
of  the  flexors  of  the  leg.  (Anesthesia,  see  Fig.  25,  pero- 
neal, anterior  cutaneous,  and  plantar  nerves.)  Irritative 
symptom  in  the  sensory  fibers  of  the  nerve,  sciatica. 


\.lfcnirat 


cp. 


!  • 


■adduct  m, 
■CbuLdn^;  f 


M 


■..    ?. 


,\X 


sural.. 


% 


xtu/uu 


Fig.  25. 


•cole 
plant  J.-  —^^X^;^'Plam.  n 

-ii,    Ilio-inguinal ;    sp.e,  external   spermatic;    ih,    iliohypo- 
gastric; C.JO,  posterior  cutaneous. 


14.  Peroneal  Nerve. — Paralysis  of  the  peronei,  tibialis 
anticus,  extcnsores  digitorum  et  hallucis.  Inability  to  flex 
the  foot  on  the  leg  (foot-drop).  The  outer  border  of  the 
foot  is  lower  than   the   inner   border.     Contractures  in 


DISEASE  OF  THE  SYMPATHETIC  NERVE.  103 

antagonistic  muscles  (muscles  of  the  calf)  ;  talipes  equinus 
or  talipes  varus  (if  the  extensor  digitorum  only  is  involved) 
may  be  produced.      (Anesthesia,  see  Fig.  25,  peroneus.) 

15.  Tibial  Nerve. — Paralysis  of  the  muscles  of  the 
calf;  plantar  flexion  impossible  ;  inability  to  flex  the  toes. 
By  contractures  in  the  antagonistic  muscles  (peronei  exten- 
sors) talipes  calcaneus  is  produced.  (For  anesthesia  see 
Fig.  25,  plantar  nerve.) 

D.    Symptoms  of  Disease  of  the  Sympathetic  Nerve. 

The  paralytic  symptoms  in  lesions  of  the  cervical  por- 
tion are  the  following : 

Miosis,  diminution  in  the  palpebral  fissure,  retraction 
of  the  bulb,  oculopupillary  symptoms  (fibers  from  the  first 
dorsal  segment,  see  p.  94).  Anomalies  in  the  sweat  secre- 
tion of  the  corresponding  half  of  the  body.  Among  the 
irritative  symptoms  have  been  mentioned  dilatation  of  the 
pupil  and  disturbances  in  the  circulation.  Disease  of  the 
cardiac  and  splanchnic  branches  gives  rise  to  disturbances 
in  the  cardiac,  intestinal,  and  glandular  functions,  our 
knowledge  of  which  is  very  imperfect.  The  nature  of  the 
disturbance  appears  to  be  chiefly  motor,  possibly  also  to 
some  extent  secretory. 


II.  THE  SYMPTOMS  OF  SYSTEM  DISEASES. 

The  term  system  diseases,  as  has  been  mentioned,  is 
applied  to  symmetric  processes  affecting  an  entire  nerve 
path,  consisting  of  functionally  and  anatomically  related 
fibers  or  neurons,  or,  at  first,  to  processes  affecting  por- 
tions of  neurons  successively.  In  the  end  the  disease 
rarely,  if  ever,  confines  itself  to  one  portion  of  the  neuron 
(cell  or  fiber),  the  entire  neuron  being  eventually  destroyed. 
The  localization  of  the  primary  seat  of  the  disease  is  often 
of  the  highest  importance  for  the  clinical  course.  Unfor- 
tunately, our  knowledge  of  the  direction  in  which  the  pro- 


104    GENERAL  PATHOLOGY  AND  TEEATMENT. 

cesses  spread  and  their  point  of  origin  is  in  many  particu- 
lars very  incomplete. 

I.  System  Diseases  of  the  Corticomuscular  Motor 
Path. —  (a)  Of  the  Central  Neuron  (Simple  Spastic 
Spinal  Paralysis). — Cases  of  this  kind  are  rare.  Ana- 
tomically we  find  a  slowly  progressing  symmetric  degen- 
eration of  the  entire  pyramidal  tract  (origin,  the  motor 
pyramidal  cells  in  the  cortex).  Clinically  we  observe  a 
slowly  increasing  spastic  paralysis  of  the  extremities,  with 
heightened  reflexes,  but  without  muscular  atrophy  and 
without  disturbances  of  sensation  or  of  the  bladder. 

(b)  Of  the  Peripheral  Neuron. — This  leads  to  flaccid 
muscular  paralysis,  with  degenerative  muscular  atrophy. 
The  reflexes  are  abolished.  The  primary  seat  may  be  in 
the  neuron  cell  or  in  the  neuron  fiber. 

a.  Primary  Cell  Diseases. — The  morbid  process  pre- 
sents a  great  variety  of  symptoms,  depending  on  the  seat 
of  the  lesion. 

Chronic  and  acute  ophthalmoplegia^  when  the  lesion  is  in 
the  nuclei  of  the  ocular  muscles. 

Bulbar  Paralysis^  Chronic  and  Acute). — The  seat  is  in  the 
bulbar  nuclei  of  the  facial,  hypoglossus,  and  trifacial  nerves. 

Spinal  Mvbscular  Atrophy, — The  legion  is  in  the  gray 
matter  of  the  anterior  horn,  particularly  in  the  cervical 
portion  of  the  cord. 

Acute  and  Chronic  Anterior  Poliomyelitis, — Inflamma- 
tory processes  in  the  gray  matter  of  the  anterior  horn, 
affecting  the  ganglion  cells. 

/?.  Primary  (?)  diseases  of  the  fibers,  neurotic  mus- 
cular atrophy,  peroneal  type  of  muscular  atrophy  (pero- 
neal, ulnar,  and  median  nerves).  Participation  of  the 
ganglion  cells  can  not  be  excluded  with  certainty. 

The  motor  form  of  multiple  neuintis  may  affect  all  the 
motor  nerves. 

y.  Progressive  Muscular  Dystrophy. — The  disease  is 
confined  to  the  terminal  portion  of  the  neuron — i,  e.,  the 
muscle. 


COMBINED  SYSTE3T  DISEASES.  105 

(c)  Of  the  Entire  Pathway. — In  these  cases  there  is 
degeneration  of  the  pyramidal  tract  and  of  the  peripheral 
nerves  (ganglion  cells  and  fiber,  peripheral  nerve) — that  is, 
amyotrophic  lateral  sclerosis  and  possibly  bulbar  paralysis. 
The  clinical  symptoms  are  those  of  spastic  paralysis  of 
the  extremities,  with  degenerative  muscular  atrophy. 

It  is  probable  that  numerous  intermediate  forms  between 
these  distinct  varieties  occur. 

2.  System  Diseases  of  the  Centripetal  Sensory- 
Path. — We  do  not  know  of  any  isolated  affections  of  the 
central  path  belonging  to  this  category.  There  is,  how- 
ever, a  degeneration  of  the  peripheral  neuron  (so-called 
tabes  dorsalis)  of  quite  frequent  occurrence,  in  which  the 
neuron  may  be  affected  in  its  entire  extent.  In  rare  cases 
the  central  pathway  may  also  be  involved  (lateral  cerebral 
and  anterolateral  tract).  The  symptoms  consist  in  painful 
sensations  and  disturbances  of  sensation  and  coordination ; 
the  reflexes  are  abolished.  This  category  also  includes 
the  sensory  form  of  multiple  neuritis. 

3.  The  Combined  System  Diseases. — These  include 
degenerative  processes  affecting  simultaneously  both  the 
motor  and  the  sensory  paths. 

(a)  Hereditary  or  Friedreich's  Ataxia. — The  central 
motor  neuron  (pyramidal  tract)  and  the  peripheral  and 
central  sensory  neuron  (posterior  columns,  cerebral  lateral 
tracts)  are  diseased.  (For  symptoms  see  Special  Path- 
ology.) 

(b)  Tabes  combine,  or  true  tabes,  with  participation  of 
the  lateral  pyramidal  tracts,  frequently  with  participation 
of  other  neurons — for  instance,  peripheral  motor  neurons 
(oculomotor,  abducens,  etc.). 

(c)  Another  class  of  morbid  diseases,  better  known  ana- 
tomically than  clinically  (posterior  columns,  lateral  cere- 
bellar tract,  pyramidal  tract).  Whether  other  cerebral 
tracts  may  become  the  primary  seat  of  system  disease  is 
not  known. 


106    GENERAL  PATHOLOGY  AND  TREATMENT. 

4.  General  Considerations   on  Methods  of  Exami- 
nation and  Diagnosis. 

1.  Before  proceeding  with  the  examination,  the  history- 
should  be  carefully  taken,  as  it  is  often  of  the  greatest 
assistance  in  the  diagnosis.  Among  others,  the  following 
points  should  be  carefully  determined  : 

(a)  Heredity  (nervous  diseases,  consanguinity  of  the 
parents,  psychosis,  alcoholism,  suicide,  tuberculosis,  and 
syphilis). 

(6)  The  previous  history  of  the  patient  in  regard  to 
mode  of  life  and  habits  (education,  temperament,  alcohol, 
tobacco,  morphin,  excesses  of  every  kind) ;  occupation 
(overexertion,  manual  work,  lead,  arsenic) ;  former  dis- 
eases (psychic  and  bodily  injuries,  acute  infectious  diseases, 
tuberculosis,  and  syphilis). 

(c)  The  history  of  the  present  disease,  its  cause,  mode 
of  origin,  and  course. 

2.  The  examination  of  the  nervous  system  should  in 
every  instance  be  preceded  by  a  careful  examination  of 
the  general  condition  and  of  the  state  of  the  more  impor- 
tant internal  organs  (nutrition  and  vigor,  lung,  heart, 
abdominal  functions,  pulse,  urine).  Particular  attention 
should  be  paid  to  symptoms  of  syphilis,  tuberculosis,  pur- 
ulent foci,  malignant  tumors,  bone  diseases,  diabetes,  aural 
and  ocular  diseases. 

I.  The  Examination  of  the  Motor  Sphere. 

This  includes  :  1.  The  external  condition  of  the  mus- 
cles (atrophy,  hypertrophy,  folds  in  the  muscles),  to  deter- 
mine which,  by  inspection,  the  examiner's  eye  must  be 
trained  by  constant  study  of  the  normal  body.  Atrophy- 
in  the  muscles  of  the  hand,  peroneal  atrophy,  facial  par- 
alysis, atrophy  of  the  shoulder-girdle,  abnormal  position 
of  the  extremities,  etc.,  can  be  seen  at  the  first  glance. 
This  part  of  the  examination  should  include  measurement 


EXAMINATION  OF  THE  MOTOR  SPHERE.  107 

of  the  atrophied  extremities  with  a  tape-measure  and  com- 
parison with  the  sound  side. 

2.  Examination   for  Motor  Irritative  Symptoms. — 

These  inchide  tremors  of  the  extremities  (alcoholism,  mor- 
phinism, neurasthenia,  Basedow's  disease) ;  we  distinguish 
line  tremors,  up  to  twenty  a  second,  and  slow  tremors,  up  to 
six  vibrations  a  second.  Special  forms  are  the  tremor  of 
paralysis  agitans,  the  intention  tremor  in  multiple  sclero- 
sis, which  is  rather  a  disturbance  of  coordination,  and 
nystagmus  of  the  eye  muscles.  Spasms  of  individual 
muscles  or  muscle  groups,  either  clonic  (interrupted)  or 
tonic  (uninterrupted),  and  tetanoid  or  tonic  spasm  of  all 
the  muscles  of  the  body.  A  contracture  is  a  permanent 
tonic  condition  of  spasm.  A  convulsion  is  a  form  of 
extensive  tonic  or  clonic  spasm  ;  epileptiform  convulsions 
are  periodic  convulsions  (also  hysteric  convulsions).  Cho- 
reic movements  are  involuntiiry,  but  not  brusque,  like  true 
convulsions  ;  the  movements  are  irregular  and  occur  in  the 
quiescent  state.  Afhetoid  movements  are  similar,  but  extra- 
ordinarily exaggerated  movements,  occurring  especially  in 
the  fingers  and  toes.  These  conditions  may  be  present  in 
cortical  lesions  or  after  apoplexies,  but  may  also  occur 
without  apparent  cause. 

Fibrillary  muscular  contractions  have  been  referred  to 
on  page  83. 

3.  The  Examination  of  Motor  Power. — The  power  of 
each  of  the  more  important  muscles  should  be  tested  sepa- 
rately. For  estimating  the  power  of  some  of  the  muscles, 
as  those  used  in  gripping,  we  have  the  dynamometer,  but 
in  most  cases  the  strength  of  the  muscle  is  determined 
by  comparing  it  with  that  of  the  other  side  and  by  the 
resistance  offered  to  the  hand  of  the  examiner.  Pro- 
ficiency in  this  respect  can  only  be  acquired  by  long 
practice. 

The  functions  of  all  the  muscles  are  tested  in  the  order 
of  the  motor  nerves,  beginning  with  the  eye  muscles.  (See 
Plate  27.)     The  extent  and  force  of  both  active  and  pas- 


108    GENERAL  PATHOLOGY  AND  TREATMENT. 

sive  movements  should  be  determined,  the  attention  being 
specially  directed  to  the  joints. 

It  is  exceedingly  important  to  examine  the  gait : 
whether  it  is  paretic  or  laborious,  as  a  result  of  muscular 
weakness ;  spastic,  on  account  of  abnormal  muscular  stiff- 
ness ;  ataxic,  from  disturbance  of  the  coordination  ;  hemi- 
plegic,  the  patient  dragging  one  of  his  legs  and  advancing 
the  other  by  a  movement  of  adduction  instead  of  raising 
the  foot  (in  central  paralysis) ;  or,  finally,  peroneal,  the 
tips  of  the  toes  dragging  on  the  ground  because  the  peronei 
are  paralyzed. 

4.  Examination  of  the  Power  of  Coordination. — This 
is  done  by  requiring  the  patient  to  carry  out  complicated 
movements  of  the  arms,  such  as  bringing  the  tips  of  the 
fingers  together,  and  various  movements  of  the  legs.  If 
the  nicety  of  the  movements  is  impaired,  the  condition  is 
termed  ataxia.  It  occurs  in  multiple  sclerosis,  tabes  dor- 
salis,  hereditary  ataxia,  multiple  neuritis,  etc.  Static  co- 
ordination (attitude  of  the  trunk)  is  tested  by  requiring 
the  patient  to  stand  with  his  eyes  closed  ;  swaying  under 
these  conditions  is  known  as  Romberg's  sign.  In  cere- 
bellar ataxia  the  gait  resembles  that  of  a  drunken  man  and 
is  very  characteristic. 

5.  Examination  of  the  Electric  Condition  of  the 
Muscles. 

Electric  Diagnosis. — This  is  a  diagnostic  procedure 
of  the  greatest  value.  In  the  electric  examination  we 
utilize  the  galvanic,  primary,  or  constant  current ;  or  the 
faradic,  induced,  seccmdary,  or  interrupted  current.  The 
galvanic  is  the  more  important. 

(a)  Galvanic  Examination. — The  usual  apparatus  con- 
tains : 

1.  Cells  containing  J  ^"""^^^  ^  ""^^^       I  Carbon  in  HNO3. 

two  fluids.         /  ri^ovp'«*  ppU  /  ^^"^  ^^  H,SO,. 

I  ^rove  s  cell  j  Platinum  in  HNO3. 

2.  Cells  with  only  |  Leclanche's  cell  {  ^^^^^^  (Braunstein)  ^  ^Cl,. 

one  fluid.  I  Bunsen's  cell       {  ^^^^^^  in  KMnO,  4-  H^SO,, 


ELECTRIC  DIAGNOSIS.  109 

with  the  addition  of  sulpliid  of  mercury  to  replace  the 
used-up  zinc  amalgam. 

The  chemic  processes  (formation  of  a  salt)  that  are 
set  up  in  these  cells  produce  a  difference  in  the  electric 
potential  between  the  two  poles,  the  zinc  pole  (negative 
pole,  oxygen  pole)  and  the  carbon  pole  (positive  pole, 
hydrogen  pole),  and  the  neutralization  of  this  difference 
by  wire  connections  produces  the  galvanic  electric  current. 

The  current  flows  from  the  positive  pole  (anode)  to  the 
negative  pole  (cathode) — that  is  to  say,  from  the  carbon  to 
the  zinc.  To  assist  the  memory  it  may  be  remembered 
that  C  conies  before  Z.  The  electromotive  force  depends 
on  two  conditions  :  the  internal  resistance  offered  by  the 
cells  and  the  external  resistance  that  the  current  has  to 
overcome.  The  dry  skin  of  a  human  being  at  first  offers 
a  very  great  resistance  when  it  is  included  in  the  circuit. 
After  a  time  the  resistance  diminishes  and  is  finally  over- 
come, the  current  passing  without  interruption. 

The  strength  of  the  current  is  measured  by  means  of 
the  galvanometer,  and  is  expressed  in  milliamperes,  an 
arbitrary  unit  which  has  now  come  into  general  use. 

The  strength  of  the  current  can  be  graduated  by  means 
of  rheostats  (the  addition  of  resistance  coils). 

The  healthy  muscle,  when  irritated  with  the  galvanic 
current,  reacts  with  a  rapid  and  lightning-like  contraction, 
both  on  opening  and  closing  the  current,  the  contractions 
taking  place  in  the  following  order  as  the  strength  of  the 
current  is  increased  : 

On  cathodal  closing,  CCl ;  anodal  closing,  ACl ;  anodal 
opening,  AO  ;  and,  finally,  on  cathodal  opening,  CO. 

If  the  current  is  still  further  increased,  a  tetanic  con- 
traction takes  place  (CClTe  before  AClTe). 

When  the  muscle  is  degenerating  the  electric  reactions 
are  somewhat  different.  The  contraction  does  not  take 
place  abruptly  and  like  a  flash  of  lightning,  but  slowly, 
sluggishly,  and  in  distinct,  visible  waves.  In  addition, 
anodal  closing  contraction  takes  place  before  the  cathodal 


110     GENERAL  PA THOLOG  Y  AND  TREA TMENT. 

contraction.     This  morbid  condition  is  designated  as  the 
7'eaction  of  degeneration  (RD). 

As  degenerative  muscular  atrophy  only  occurs  in  lesions 
of  the  peripheral  motor  neuron  (see  p.  83),  the  presence 
of  pronounced  reaction  of  degeneration  affords  a  sure 
means  of  distinguishing  central  disease  from  disease  of  the 
peripheral  motor  neuron.  Reaction  of  degeneration  takes 
place  whether  it  is  the  cell  or  the  fiber  of  the  peripheral 
neuron  that  is  the  first  to  become  diseased. 

We  distinguish  between  complete  and  partial  reaction 
of  degeneration.  In  complete  reaction  of  degeneration  the 
muscle  can  not  be  stimulated  through  the  nerve  (indirect 
stimulation),  and  if  the  muscle  is  stimulated  directly,  the 
reactions  of  degeneration  ensue.  If  the  degenerative  atro- 
phy has  run  its  course  and  the  muscle  is  completely  con- 
verted into  connective  tissue  (sclerosis),  even  the  reactions 
of  degeneration  disappear  in  direct  stimulation.  If  the 
muscle  recovers,  however,  the  reactions  of  degeneration 
disappear,  the  contractions  become  normal,  and  the  muscle 
responds  to  stimulation  of  the  nerve  (indirect  stimulation), 
even  before  the  reaction  of  degeneration  disappears. 

In  partial  reaction  of  degeneration  the  muscle  can  still 
be  stimulated  through  the  nerve,  and  the  reaction  of  degen- 
eration ensues  when  the  muscle  is  stimulated  directly. 
This  form  occurs  in  milder  lesions.  Thus,  the  examina- 
tion with  a  galvanic  current  enables  us  not  only  to  localize 
the  disturbance  (peripheral  neuron),  but  also  to  determine 
the  severity  of  the  lesion — in  other  words,  the  prognosis. 

If  in  any  case  of  muscular  paralysis  due  to  a  lesion  of 
the  peripheral  neuron  the  reactions  of  degeneration  do  not 
make  their  appearance  within  a  few  days,  a  complete  cure 
may  be  expected  in  the  course  of  a  few  days  or  weeks  (mild 
form).  If  partial  reactions  of  degeneration  take  place,  the 
paralysis  will  last  not  less  than  several  months  (medium 
form).  If  complete  reactions  of  degeneration  occur,  re- 
covery may  take  place  after  several  months  (four  to  nine). 
On  the  other  hand,  the  paralysis  may  be  permanent  (dis- 


EXAMINATION  WITH  THE  FARADIC  CURRENT.      Ill 

appearance  of  the  reactions  of  degeneration — severe  form). 
The  last-named  result  can  not  be  predicted  with  certainty. 
The  reactions  of  degeneration  occur  in  conjunction  with 
fibrillary  muscular  contractions  and  an  atrophy  in  all 
nuclear  lesions  of  the  peripheral  neuron  (spinal  muscular 
atrophy,  anterior  poliomyelitis,  amyotrophic  lateral  scle- 
rosis, myelitis,  etc.) ;  in  all  severe  lesions  of  the  anterior 
roots  and  of  the  peripheral  nerves  (neuritis,  compression, 
traumatism).  In  addition  to  the  qualitative  alteration 
there  may  also  be  a  quantitative  change,  in  the  form  of 
either  a  morbid  diminution  or  heightening  of  the  excita- 
bility of  the  muscle.  This  quantitative  difference,  how- 
ever, has  not  the  same  significance  as  the  qualitative 
changes.  Before  we  proceed  with  the  explanation  of  this 
alteration  we  will  describe  briefly — 

(b)  Examination  with  the  Faradic  Current.  —  The 
faradic  or  induction  apparatus  in  common  use  contains, 
in  addition  to  the  galvanic  cells  that  produce  the  necessary 
primary  current  (usually  the  modified  Leclanch^  and 
Bunsen),  a  DuBois  Reymond  induction  coil  consisting  of 
two  movable  w  ire  coils.  The  primary  current  is  produced 
in  the  primary  coil  and  generates  by  induction  a  secondary 
current  in  the  secondary  coil,  placed  above  the  primar}^  coil, 
the  induced  current  flowing  in  the  opposite  direction  to 
the  primary. 

By  means  of  an  interrupter  (Wagner  hammer)  the 
primary  current  is  constantly  interrupted,  and  its  direc- 
tion changed  by  means  of  an  electromagnet.  In  this  way 
a  series  of  secondary  currents  are  induced  in  the  induction 
coil,  always  in  the  opposite  direction  and  also  alternating, 
the  strength  of  the  current  being  regulated  by  the  dis- 
tance between  the  secondary  and  the  primary  coils.  The 
strength  of  the  current  is  read  in  centimeters  of  the  dis- 
tance between  the  coils ;  the  greater  the  distance,  the 
weaker  the  current.  When  the  reactions  of  degeneration 
are  present  imder  stimulation  with  the  galvanic  current, 
the  muscle  fails  to  respond  either  to  nervous  or  to  mus- 


112     GENERAL  PATHOLOGY  AND  TREATMENT. 

cular  irritation  with  the  faradic  current.  If  recovery  takes 
place,  the  muscle  responds  somewhat  earlier  to  indirect 
than  to  direct  stimulation. 

In  regard  to  the  quantitative  changes  in  the  irritability, 
it  is  to  be  remembered  that  the  various  nerves  and  muscles 
require  varying  strengths  of  current  for  their  stimulation, 
depending  on  their  position  and  composition.  Hence  one 
must  know  the  average  strength  required  to  stimulate  the 
normal  muscle  in  order  to  be  able  to  determine  whether 
there  is  any  morbid  quantitative  alteration  in  the  excita- 
bility. The  necessary  current  strength  for  the  various 
nerves  and  muscles  is  determined  at  definite  points, — the 
motor  points, — ^and  for  electrodes  of  a  definite  size  (normal 
electrode,  3  sq.  cm.).  The  most  important  figures  in  mil- 
liamperes  for  the  normal  galvanic,  and  in  centimeters  for 
the  distance  between  the  coils  for  faradic,  irritability  of  the 
nerves  are  the  following,  taken  from  Stintzing  (the  figures 
for  the  muscles  are  comparatively  unimportant)  : 

Galvanic.  Faradic. 

Facial  nerve 1.75  ma.  121  cm. 

Frontal  branch  ....   1.45   "  128   " 

Mental  branch   ....   0.95    "  132    " 

Spinal  accessory  nerve     .    .    .   0.27    "  137   " 

Median  nerve  (in  the  arm)     .0.9     ''  122    " 

Ulnar  nerve 0.55    "  130    '' 

Radial  nerve 1.8     ''  105    " 

Crural  nerve 1.05    "  111    '' 

Peroneal  nerve 1.1      "  115    " 

Morbid  increase  in  the  galvanic  excitability  occurs  espe- 
cially in  conjunction  with  the  reactions  of  degeneration, 
and  without  the  reactions  of  degeneration  in  tetany,  my- 
elitis, etc.  (also  of  faradic  excitability).  Diminution  in 
the  electric  excitability  accompanies  all  the  forms  of 
simple  atrophy  (central  palsies).  Morbid  diminution  in 
the  resistance  of  the  skin  occurs  in  Basedow's  disease,  in 
which  the  skin  is  abnormally  moist. 


EXAMINA  TION  OF  THE  SENSOE  Y  SPHERE.  113 

II.   Examination  of  the  Sensory  Sphere. 

1.  Subjective  Symptoms. — These  include  all  the 
statements  of  the  patient,  either  spontaneous  or  in  answer 
to  inquiry,  of  painful  sensations  of  every  kind,  their  local- 
ization, character,  and  duration.  We  distinguish  genuine 
pain  (cause,  mechanical,  inflammatory,  or  toxic  irritation 
of  the  sensory  nerves)  and  indefinite  pain  of  longer  dura- 
tion, such  as  headache  and  cardiac  and  gastric  distress. 
Different  from  either  of  these  varieties  is  the  central  psy- 
chic pain  that  occurs  in  neuroses  and  psychoses  and  can 
not  be  localized. 

In  this  category  belong  also  paresthesias  or  abnormal 
sensations,  such  as  burning,  furry  feeling,  formication, 
occurring  in  neurasthenia,  neuritis,  tabes,  myelitis,  etc. 
Insomnia  occurs  when  the  nervous  system  is  either  ex- 
hausted or  abnormally  excited.  Vertigo  is  observed 
chiefly  in  circulatory  disturbances  of  the  brain  (hyperemia, 
anemia,  arteriosclerosis,  epilepsy),  in  neurasthenia,  and  in 
diseases  of  the  eye  and  ear. 

2.  Objective  Examination  of  the  Various  Modes 
of  Sensation  in  the  Skin. — (a)  Tactile  Sense. — The 
same  examination  serves  to  determine  both  the  tactile  and 
the  pressure  sense  of  the  skin.i  The  patient  is  asked  to 
distinguish  between  contact  with  the  point  and  the  head 
of  a  pin,  or  with  a  cotton  pellet  or  the  examiner's  fingers. 
He  should  be  told  to  answer  '^  now  "  whenever  he  feels 
the  test-object.  In  order  to  test  the  patient's  attention  it 
is  well  to  make  occasional  '^  blind  tests,''  taking  care  not 
to  fatigue  the  patient  unduly.  The  examination  should 
be  repeated  frequently  at  diiferent  times.  If  possible,  the 
diseased  side  should  be  compared  with  the  sound  side  of 
the  body  by  going  over  all  the  various  regions  of  the  skin. 

^  The  skin  contains  various  sensory  points  or  areas,  where  sensation 
for  the  different  modes  of  sensation  is  concentrated.  Thus,  we  speak 
of  thermic  areas,  pressure  areas,  and  pain  areas  ;  the  last-named  are 
the  most  numerous. 

8 


Fig.  26.— Cutaneous  areas  corresponding  to  the  sensory  segments 
of  the  spinal  cord  :  A,  Anterior,  B,  posterior,  surface  (after  Sticker, 
"Munch,  med.  Wochenschr.,"  1896,  p.  194).   See  also  Fig.  17. 

114 


EXAMINATION  WITH  THE  F ARABIC  CURRENT.     115 

It  may  be  useful,  also,  to  test  the  sensitiveness  of  the  skin 
to  faradic  stimulation,  the  strength  of  current  being  indi- 
cated by  the  number  of  centimeters  measuring  the  distance 
between  the  coils.  There  may  be  anesthesia,  or  total  aboli- 
tion of  the  tactile  sense,  when  there  is  complete  interruption 
of  the  sensory  pathway,  especially  in  focal  diseases  (see  3  in 
this  chapter)  and  in  hysteria  of  central  origin.  Hypesthesia, 
or  diminution  in  the  tactile  sense,  when  there  is  a  partial 
interruption  of  the  sensory  path,  as  in  neuritis,  tabes,  etc.; 
hyperesthesia,  or  morbid  exaggeration  of  sensation.  (See 
under  Pain  Sense.)  The  extent  of  the  anesthetic  areas 
should  be  carefully  outlined.  In  lesion  of  a  peripheral  nerve 
it  will  be  found  to  correspond  to  the  distribution  of  the 
nerve.  (See  Figs.  2e3,  24,  and  25.)  In  diseases  of  the 
spinal  cord  the  anesthetic  area  will  be  found  to  extend  as 
high  up  as  the  cutaneous  area  supplied  by  the  uppermost 
segment  involved.     (See  Fig.  26  and  under  b.) 

(b)  Localization  of  Sensations  (Topographic  Sense). — 
This  is  tested  at  the  same  time  as  the  tactile  sense.  The 
patient,  having  been  blindfolded,  is  asked  to  indi(;ate  the 
precise  spot  where  he  feels  the  sensation. 

The  power  of  feeling  two  contact  points  on  the  skin  at 
a  given  distance  from  each  other  is  tested  by  means  of  a 
pair  of  compasses.  The  following  table,  taken  from  Weber, 
indicates  the  distances  in  millimeters  at  which  the  points 
of  the  compass  are  felt  as  two  distinct  points  in  different 
parts  of  the  body  ; 

Tip  of  the  tongue   .    .    1  mm.  Arm       65  mm. 

Lips  (muc.  mem.)      .    4  ''  Forearm 39  '' 

Tip  of  the  nose  .    .    .    6.5  "  ^^.    j   volar    .    .    .  11 .  " 

Cheeks      11  ''  ^^"^    1   dorsal      .    .  28  " 

Forehead      30  "  Tip  of  finger   ....    2  " 

Chest 44  "  Thigh 65  " 

Middle  of  back  ...  65  ''  Leg    . 39  '' 

Buttocks 39  ''  Tip  of  toe 11  '' 

The  lower  the  number,  the  greater  the  sensitiveness  of 
the  corresponding  region.  In  polyesthesia  the  patient  mis- 
takes a  single  contact  for  several  (tabes). 


116  GENERAL  PA THOLOG Y  AND  TREA TMENT. 

(c)  Pain  Sense. — The  pain  sense  in  the  individual 
regions  of  the  body  is  tested  by  inserting  a  needle  to 
various  depths.  The  sense  can  be  accurately  measured 
with  the  faradic  current,  the  strength  of  the  current  being 
increased  up  to  the  point  of  painfulness.  It  is  only  called 
for,  however,  in  very  delicate  clinical  examination.  The 
pain  sense  may  be  diminished  {liypalgesia)  or  abolished 
altogether  {analgesia). 

Analgesia  occurs  in  association  with  loss  of  the  tactile 
sense  in  focal  diseases,  hysteria,  tabes  dorsalis,  and,  by 
tumors,  in  syringomyelia. 

The  pain  sense  may  be  delayed — that  is,  it  may  require 
for  its  perception  a  summation  of  protracted  stimuli  (in 
tabes,  myelitis,  and  neuritis).  When  this  is  the  case,  the 
patient  first  announces  that  he  feels  the  contact  of  the 
object,  and  later  expresses  the  painful  sensation  by  an 
exclamation,  as  "  Now  ! ''  '^  Ouch  !  '^  Abnormally  pro- 
tracted pain  sense  occurs  in  tabes  and  neuritis. 

Hyperalgesia,  or  abnormal  sensitiveness  to  contact  and 
thermic  stimuli,  occurs  as  an  irritative  symptom  in  focal 
diseases,  in  hysteroneurasthenia,  in  lesions  of  one  side  of 
the  cord,  and  in  neuritis. 

(d)  Temperature  Sense. — Cold  and  heat  perception  is 
to  be  tested  separately,  with  test-tubes  filled  with  iced 
water  and  with  warm  water  (not  hot).  The  temperature 
sense  may  be  blunted  or  abolished.  Thermo-anesthesia  for 
both  hot  and  cold,  or  for  either  alone,  occurs  in  focal  dis- 
eases, tabes,  syringomyelia,  myelitis,  and  neuritis.  The 
two  sensations  may  be  mistaken  for  one  another — per- 
verted temperature  sense  (tabes,  myelitis,  neuritis). 

3.  Sensation  in  the  Deeper  Parts  of  the  Body. — 
(a)  The  sense  of  weight  is  tested  by  applying  different 
weights  wrapped  up  in  cloths  and  comparing  the  results 
with  those  obtained  in  a  normal  subject. 

(b)  The  power  of  perceiving  passive  motions  is  tested 
by  performing  some  slight  passive  movement  and  requir- 
ing the   patient,   who   has  been  blindfolded,  to   indicate 


METHODS  OF  TESTING    THE  SPECIAL  SENSES.     117 

whether  the  limb  has  been  flexed,  extended,  raised,  ab- 
ducted, etc. 

(c)  The  sense  of  position  is  tested  by  placing  an  arm 
or  a  leg  in  a  certain  position,  and,  after  blindfolding  the 
patient,  asking  him  to  imitate  it  with  the  other  extremity. 

These  disturbances,  together  with  others  that  are  diffi- 
cult to  test,  such  as  sensations  in  the  limbs  and  muscles, 
are  designated  as  disturbances  of  the  musde  sense ;  they 
occur  in  tabes,  hereditary  ataxia,  hysteria,  and  in  focal 
diseases. 

4.  Methods  of  Testing  the  Special  Senses. — 
(a)  The  Sense  of  Sight. — Each  eye  and  the  homologous 
halves  of  the  retina  are  to  be  tested  separately.  In  some 
cases  it  is  necessary  to  determine  the  visual  acuity  and  the 
extent  of  the  visual  field  by  means  of  the  perimeter.  For 
this  the  reader  is  referred  to  text-books  on  ophthalmology. 
An  approximate  idea  of  the  size  of  the  visual  field  can  be 
obtained  by  gradually  bringing  the  hand  or  test-card  into 
the  visual  field,  while  the  patient  keeps  his  eyes  fixed.  If, 
for  instance,  when  the  hand  is  approached  from  the  left 
side  of  the  patient  toward  the  median  line  and  is  not  per- 
ceived with  both  eyes  before  it  reaches  the  middle  line, 
while  on  the  right  side  the  hand  is  perceived  before  it 
reaches  the  middle  line,  there  exists  left-sided  bilateral 
homonymous  hemianopsia  (the  lesion  is  located  in  the 
optic  tract  of  the  right  side,  the  primary  optic  centers,  the 
optic  radiation,  or  the  occipital  lobe  of  the  right  side).  In 
the  same  way  concentric  contraction  of  the  visual  field  or 
central  defects  (scotomata)  may  be  roughly  determined. 
Failure  to  perceive  a  visual  impression  in  both  temporal 
halves  of  the  visual  field  (bitemporal  hemianopsia)  points 
to  an  affection  of  the  chiasm.  In  injury  of  the  optic 
nerve  there  is  more  or  less  amblyopia  or  amaurosis  of  the 
corresponding  eye.  (In  regard  to  diplopia  see  under 
Paralysis  of  the  Ocular  Muscles.) 

Examination  of  the  eye-ground  by  means  of  the  oph- 
thalmoscope is  indispensable  in  any  grave  disease  of  the 


118  GENERAL  PATHOLOGY  AND  TREAT3IENT. 

nervous  system.  It  may  elicit  the  important  sign  of 
choked  disc.  This  phenomenon  is  due  to  obstruction  of 
the  lymphatic  flow  in  the  sheath  of  the  optic  nerve,  which 
occurs  when  the  intracranial  tension  is  increased,  as  by 
tumors.  A  similar  condition,  known  as  optic  neuritis, 
in  which  the  exudation  is  less  profuse,  may  also  occur  in 
intracranial  tumors  and  in  multiple  neuritis,  brain  syph- 
ilis, meningitis,  etc.  It  may  end  in  atrophy  of  the  optic 
nerve,  manifesting  itself  in  pallor  of  the  papilla,  which  is 
sharply  outlined. 

Atrophy  of  the  optic  nerve  also  occurs  primarily  in 
tabes,  multiple  sclerosis,  and  paralytic  dementia. 

(b)  Ths  Sense  of  Hearing. — Each  ear  is  to  be  tested 
separately  with  a  watch  (normal  distance,  3  meters  and 
over)  or  by  the  patient's  ability  to  hear  whispering  at 
even  greater  distances. 

To  determine  whether  the  deafness  is  due  to  disease  of 
the  labyrinth  or  of  the  sound-conducting  organs  (middle 
ear),  the  tuning-fork  test  is  employed.  If  a  tuning-fork 
be  first  placed  on  the  head,  and  as  soon  as  it  ceases  to  be 
heard  by  bone  conduction  be  held  before  the  patient's  ear, 
one  of  the  two  following  results  will  be  obtained :  (1 )  either 
the  sound  will  again  be  heard  (positive  Rinne),  in  which 
case  the  disease  is  situated  in  the  labyrinth  (meningitis, 
disease  of  the  auditory  nerve),  or  (2)  the  tuning-fork  will 
not  be  heard  (negative  Riinie) — a  sign  of  middle-ear 
involvement. 

In  sev^ere  grades  of  nervous  deafness  bone  conduction 
disappears  entirely. 

Paresthesias  of  the  sense  of  hearing  occur  in  the  form 
of  buzzing  and  ringing  sounds  in  otitis,  Meniere's  symp- 
tom-complex, anemia,  etc.  ;  auditory  hyperesthesia,  in 
which  sound  perception  is  accompanied  by  pain,  occurs  in 
hysteria,  hemicrania,  etc. 

(c)  The  Sense  of  Smell. — The  two  halves  of  the  nose 
are  tested  separately  by  means  of  some  odoriferous  sub- 
stances, care  being  taken  to  avoid  any  substance,  such  as 


EXAMINATION  OF  THE  REFLEXES.  119 

ammonia,  which  would  irritate  the  trifacial  nerve.  Oil 
of  peppermint,  balsam  of  Peru,  oil  of  almond,  and  asa- 
fetida  may  be  used.  Excluding  for  the  present  diseases 
of  the  nasal  mucous  membrane,  anosmia  occurs  in  periph- 
eral lesions  (tumors,  injury  of  the  anterior  fossa  of  the 
skull,  atrophy  of  the  olfactory  nerve) ;  central  disturb- 
ances are  rarely  seen  except  in  hysteria. 

(d)  The  Sense  of  Taste. — The  two  halves  of  the  tongue 
should  be  tested  separately  in  the  anterior  two-thirds  (tri- 
facial) and  posterior  third  (glossopharyngeal)  by  applying 
sapid  substances,  such  as  solutions  of  common  salt,  sugar, 
vinegar,  or  qiiinin.  Ageusia,  or  loss  of  the  sense  of  taste, 
occurs  in  lesions  of  the  peripheral  nerves  (facial  in  the 
Fallopian  canal ;  trifacial),  in  hysteria,  and  rarely  in  central 
lesions. 

III.   Examination  of  the  Reflexes. 

The  reflexes  may  be  heightened,  diminished,  or  abol- 
ished. 

Increase  in  the  reflexes  depends  either  on  failure  of  the 
inhibition  through  the  central  pathways,  as  in  exhaustion, 
neurasthenia,  or  disease  of  the  inhibitory  pathway,  or  on 
abnormal  irritability  within  the  reflex  arc,  as  in  neuritis, 
meningitis,  tetanus.  Diminution  or  abolition  of  the  reflexes 
occurs  when  the  reflex  arc  is  interrupted,  whether  in  the 
sensory  or  motor  portion  or  in  the  connecting  link  formed 
by  the  reflex  collaterals ;  reflexes  are  also  absent  in  deep 
coma  and  in  intoxications.  In  marked  exaggeration  of 
the  tendon  reflexes  continuous  stimulation  produces  a  rapid 
succession  of  reflex  contractions  (patellar  clonus,  ankle- 
clonus).  The  most  important  reflexes  to  examine  are  the 
following  : 

1.  Cutaneous  Reflexes  and  Reflexes  of  the  Mucous 
Membrane. — The  plantar  reflex  and  the  reflex  sensibility 
of  the  tips  of  the  fingers  are  tested  with  a  needle,  by  con- 
tact with  heat  or  cold,  or  by  tickling  the  part  (summated 
impulses). 


120    GENERAL  PATHOLOGY  AND  TREATMENT. 

The  pathway  of  these  reflexes  is  imperfectly  known  ; 
the  sensory  branch  appears  to  communicate  by  means  of 
collateral  and  reflex  neurons  (long  reflex  arc)  with  the 
entire  motor  sphere. 

In  unilateral  lesions  interrupting  the  pyramidal  tract 
the  cutaneous  reflexes  are  frequently  diminished,  while  the 
tendon  reflexes  are  exaggerated. 

The  cremaster  reflex,  or  contraction  of  the  cremaster 
muscle  following  irritation  of  the  inner  surface  of  the 
thigh,  and  the  abdominal  reflex,  contraction  of  the  abdom- 
inal muscles  at  various  levels  (upper  and  lower  reflex),  elic- 
ited by  stroking  the  skin  of  the  abdomen,  are  of  very  little 
clinical  significance,  so  far  as  we  know.  Both  reflexes 
appear  to  be  absent  in  focal  cerebral  lesions  on  the  side 
opposite  to  that  of  the  diseased  focus,  while  in  multiple 
sclerosis  they  are  often  absent  on  both  sides. 

The  conjunctival  reflex  consists  in  closure  of  the  lids 
when  the  conjunctiva  is  touched.  It  is  absent  in  paralysis 
of  the  trifacial  and  facial  nerves. 

The  palpebral  reflex  consists  in  closure  of  the  lids  when 
an  object  is  suddenly  brought  close  to  the  eye ;  it  is  absent 
in  lesions  of  the  optic  nerve  and  in  facial  paralysis. 

The  pharyngeal  reflex  consists  in  a  choking  movement 
following  irritation  of  the  mucous  membrane  with  a  brush  ; 
it  is  absent  in  paralysis  of  the  vagus  and  spinal  accessory. 
The  palatal  reflex  eflects  contraction  of  the  palate  after 
contact. 

2.  The  Periosteum  and  Tendon  Reflexes. — (a)  The 
patellar  tendon  reflex  is  the  most  important.  By  tapping 
the  patellar  tendon  while  the  muscles  of  the  legs  are  re- 
laxed, a  contraction  of  the  quadriceps  is  induced,  the 
patient's  attention  being  diverted  by  pressing  his  hand  or 
separating  his  folded  hands.  If  the  contractions  are  vig- 
orous, the  leg  is  jerked  forcibly  upward.  The  patient 
should  sit  on  the  edge  of  a  chair,  with  the  entire  sole  of 
the  foot  on  the  floor  and  the  leg  slightly  extended. 

The  intensity  of  the  reflex  varies  widely  within  physio- 


EXAMINATION  OF  THE  REFLEXES.  121 

logic  limits  in  various  individuals.  Exaggeration  of  the 
reflex  occurs  in  neurasthenia,  in  lesions  of  the  central  motor 
neuron  (inhibitory  fibers  in  the  pyramidal  lateral  tract), 
in  irritation  of  the  reflex  arc  (meningitis,  tetanus,  neuritis), 
and  in  exhausting  diseases.  The  reflex  is  abolished  when 
the  reflex  arc  is  interrupted  (tabes,  crural  neuritis,  anterior 
poliomyelitis,  myelitis  in  the  lumbar  enlargement),  in  coma, 
in  epileptic  attacks,  and  in  recent  injuries  of  the  spinal  cord, 
probably  as  a  result  of  irritation  of  the  inhibitory  fibers. 
(See  foot-note,  p.  93.) 

The  Achilles  tendon  reflex  is  subject  to  the  same  varia- 
tions as  the  knee-jerk.  It  consists  in  twitching  of  the 
muscles  of  the  calf  when  the  Achilles  tendon  is  tapped. 
When  this  reflex  is  exaggerated,  it  produces  the  not  unus- 
ual phenomenon  of  ankle-clonus,  elicited  by  forcible  flexion 
of  the  foot  on  the  leg.  The  more  important  of  the  peri- 
osteal and   tendon   reflexes  in  the  arm  are  the  following  : 

Radial  and  ulnar  periosteal  reflex,  elicited  by  striking 
the  styloid  process  of  the  radius  or  ulna ;  and  the  triceps 
tendon  reflex,  elicited  by  striking  the  tendon  above  the 
olecranon. 

In  addition  to  the  reflexes  mentioned,  the  masseter  reflex 
should  be  tested.  It  consists  in  a  movement  of  the  lower 
jaw,  elicited  by  striking  against  a  piece  of  wood  applied 
to  the  lower  jaw.  The  clinical  significance  of  this  reflex 
is  not  very  great.  The  pathologic  alterations  that  occur 
are  subject  in  general  to  the  above-mentioned  principles. 

3.  The  Pupillary  Reflex. — ^The  following  varieties  are 
distinguished  : 

(a)  Reaction  to  light,  or  contraction  of  the  pupil  by  the 
action  of  the  sphincter  muscle  when  the  same  eye  is  illu- 
minated (irritation  of  the  optic  nerve). 

(6)  Consensual  reaction  to  light,  which  follows  illumi- 
nation of  the  other  eye. 

(c)  Reaction  of  accommodation  or  contraction  of  the 
pupil  in  accommodating  the  eye  to  near  objects ;  really  a 
secondary  mpvement. 


122         GENERAL  PATHOLOGY  AND   TREAT3IENT. 

(d)  Converging  reaction ;  of  little  clinical  significance. 
The  contraction  is  proportionate  to  tlie  tension  of  the  rect. 
med. 

The  reaction  to  light  should  he  tested  for  each  eye  sep- 
arately, so  as  to  exclude  consensual  reaction.  If  hemi- 
anopsia is  present,  each  half  of  the  retina  should  be  tested 
separately.  It  is  best  to  use  the  ophthalmoscope,  but  for 
ordinary  purposes  it  is  enough  to  cover  the  eyes  with  both 
hands  and  then  to  remove  one  hand  quickly. 

Before  examining  the  eyes  it  is  ^^ell  to  determine 
whether  the  pupil  is  abnormally  dilated  or  contracted. 
Dilatation  (mydriasis)  occurs  in  atropinand  cocain  poison- 
ing, blindness,  coma,  epileptic  convulsions,  paralysis  of  the 
oculomotor,  and  other  conditions.  Contraction  (miosis) 
occurs  in  morphin  poisoning,  tabes,  paralytic  dementia, 
meningitis,  aifection  of  the  first  dorsal  segment,  iritis, 
etc.  Inequality  in  the  pupils,  which  occurs  in  paralysis, 
tabes,  meningitis,  and  other  conditions,  should  not  be 
overlooked. 

The  reaction  to  light  may  be  abnormally  sluggish  or 
altogether  lost  when  the  reflex  arc  is  interrupted,  as  in 
blindness  due  to  disease  of  the  optic  nerve,  in  oculomotor 
paralysis,  or  in  lesions  of  the  reflex  collaterals  (tabes, 
paralytic  dementia)  in  the  corpora  quadrigemina.  It  is 
also  observed  in  coma,  narcosis,  and  during  epileptic  con- 
vulsions, but  not  in  hysteria. 

In  lesions  of  the  optic  tract  there  is  hemianopic pupillary 
rigidity  when  the  blind  half  of  the  retina  is  illuminated. 

IV.  Examination  of  the  Functions  of  the  Bladder 
and  Rectum. 

(a)  Lesion  of  the  Central  Pathv^ays  (Myelitis  Dor= 
salis,  Focal  Diseases). — In  lesion  of  the  motor  path  there 
is  retention  of  the  urine  and  of  the  alvine  discharges  ; 
voluntary  evacuation  is  interfered  with.  If  the  bladder  is 
distended,  there  is  dribbling  of  urine. 


TROPHIC  AND  VASOMOTOR  DISTURBANCES.         123 

Lesion  of  the  sensory  paths  destroys  sensation  in  the 
bladder,  and  hence  the  desire  to  urinate,  retention  re- 
sulting. 

(b)  Lesion  of  the  peripheral  pathways  and  of  the 
bladder  center  (reflex  collaterals  in  the  sacral  portion 
of  the  cord)  produces  incontinence  of  urine  and  of  the 
alvine  discharges ;  also  sphincter  paralysis  (lesion  in  the 
lumbar  and  sacral  region  or  chorda  equina),  and  constant 
dribbling  of  urine.  The  reflex  contraction  of  the  si)hincter 
ani,  which  can  be  felt  with  the  finger  and  which  is  present 
in  central  disturbances,  is  absent. 

In  addition  to  these  paralytic  phenomena  there  may  be 
irritative  symptoms  of  a  reflex  or  central  character,  such 
as  constant  desire  to  urinate,  tenesmus,  strangnry. 

Vesical  disturbances  are  very  likely  to  resnlt  in  cystitis 
(secondary  inflammation,  polionephritis,  and  pyemia,  con- 
ditions which  always  threaten  a  patient  suffering  from 
spinal  disease). 

V.  Examination  of  Trophic  and  Vasomotor  Dis- 
turbances. 

Trophic  disturbances  occur  in  lesions  of  the  anterior 
horn,  in  neuritic  processes,  and  in  diseases  of  the  blood- 
vessels, etc.  The  most  important  symptoms  are  redness, 
swelling,  cyanosis,  abnormal  pallor,  urticaria-like  eruptions 
of  the  skin,  erythromelalgia  (painful  swelling  of  the 
hands  and  feet  occurring  in  paroxysms),  and  multiple 
cutaneous  edema.  Atrophy  of  the  skin  or  glossy  skin, 
scleroderma,  atrophy  of  the  skin  on  one  side  of  the  face 
(hemiatrophia  facialis) ;  anomalies  in  the  sweat  secretion 
(hyperhidrosis,  unilateral  sweating  in  hysteria  and  neuras- 
thenia). 

Idiopathic  gangrene  of  the  extremities  occurs  in  Ray- 
naud's disease,  syringomyelia,  and  in  Morvan's  disease ; 
bed-sores  (in  paraplegia)  are  only  indirectly  due  to  nervous 
influences.     Perforating  ulcer  in  tabes  (chronic  ulcer  in 


124    GENERAL  PATHOLOGY  AND  TREATMENT. 

the  toes) ;  alterations  in  the  joints,  arthropathies ;  swell- 
ing, thickening,  and  hypertrophy  in  tabes,  etc. 

VI.  The  Examination  of  the  Psychic  Functions. 

I.  Speech  and  Writing  (Aphasia  and  Agraphia). — 
(a)  Disturbances  of  the    Articulation  (Dysarthria). — 

By  this  term  is  meant  a  disturbance  of  the  speech  in  the 
peripheral  pathway.  There  may  be  inability  to  pronounce 
the  individual  letters  clearly,  the  pronunciation  may  be 
nasal  or  guttural  and  altogether  unintelligible,  accompa- 
nied with  great  straining  of  the  muscles  of  the  mouth  and 
tongue.  This  occurs  in  bulbar  diseases,  in  lesions  of  the 
hypoglossus  and  facial  nerve,  in  malformation  of  the  mus- 
cles used  in  speech,  absence  of  palate,  etc.  Among  special 
varieties  are  the  typical  bulbar  speech,  nasal  speech  (^rhino- 
lcdia)f  and  slow  speech  (bradylalia).  Scanning  speech 
occurs  in  multiple  sclerosis.  Halting  speech,  or  dysarthria 
Uteralis,  includes  various  defects  in  the  speech,  especially 
in  the  power  of  forming  letters. 

Stammering  is  due  to  abnormal  spastic  contractions  of 
the  muscles  of  speech,  of  central  origin.  Stammering  is 
aggravated  in  moments  of  psychic  emotion,  while  halting 
speech  is  improved.  In  disturbances  of  the  articulation  the 
labial,  dental,  palatal,  and  nasal  sounds  are  tested  separately. 

(b)  Aphasia. — Aphasia  is  always  due  to  a  central 
lesion.  It  may  be  cortical  (the  focus  is  in  the  cortex), 
transcortical  (destruction  of  the  association  fibers),  or  sub- 
cortical (interruption  in  the  motor  pathway  from  the  cen- 
ter to  the  periphery). 

a.  In  motor  or  ataxic  aphasia  the  patient  is  unable  to 
say  anything,  but  understands  everything  that  is  said  to 
him  (lesion  at  J/,  Fig.  13,  consult  p.  41). 

If  the  patient  is  unable  to  say  a  single  word  of  his  own 
accord,  there  is  total  motor  aphasia.  If  he  is  still  able  to 
say  a  few  words,  such  as  "  yes  "  and  "  no,"  the  condition 
is  known  as  m^nophasia 


APHASIA.  125 

p.  In  sensory  aphasia^  or  word-deafness  (lesion  at  J), 
the  patient  no  longer  understands  spoken  language,  but 
there  is  no  disturbance  of  the  speech-forming  apparatus. 
The  speech,  however,  is  always  impaired,  because  the  nec- 
essary association  fibers,  the  fasciculus  uncinatus  between  I 
and  II,  are  destroyed.  The  patient  either  misplaces  his 
words  or  uses  improper  words  to  express  his  ideas,  or  the 
power  of  forming  sentences  is  lost — paraphasia.  One 
form  of  this  is  the  so-called  literal  paraphasia,  or  stum- 
bling over  syllables,  in  which  letters  and  syllables  are 
misplaced  (paralytic  dementia).  When  the  memory  for 
words  is  impaired  so  that  the  patient  is  suddenly  unable 
to  think  of  a  certain  name  of  a  person  or  object,  without 
any  impairment  of  the  power  of  understanding  spoken 
language,  the  condition  is  termed  ainnedal  aphasia, 

y.  Motor  aphasia  occasionally,  and  sensory  aphasia 
very  frequently,  is  associated  with  inability  to  write, 
agraphia  (destruction  of  V  or  the  association  fibers  con- 
necting /and  //with  V;  see  Paragraphia). 

d.  A  person  who  may  or  may  not  be  the  subject  of 
sensory  aphasia  may  be  unable  to  read,  although  there  is 
no  actual  visual  disturbance.  This  condition  is  termed 
alexia.  The  lesion  is  in  the  inferior  parietal  lobe  (supra- 
marginal  convolution  ?). 

If  the  lesion  is  very  extensive,  these  phenomena  may 
be  associated  and  there  may  be  total  motor  and  sensory 
aphasia. 

£.  Mind-blindness  is  a  condition  in  which  a  patient  is 
unable  to  recognize  the  meaning  of  objects  which  he  sees 
(lesion  at  ///),  or  he  is  unable  to  find  the  right  word  for 
an  object  seen,  althougli  there  is  no  motor  aphasia.  This 
condition  is  designated  as  optic  aphasia  (interruption  of 
the  association  tracts  uniting  ///  with  /  and  //,  inferior 
longitudinal  bundle). 

Interruptions  of  the  association  tracts  uniting  /,  ///, 
and  V  produce  paragraphia,  (similar  to  paraphasia),  Avhile 
interruptions  of  the  tracts  between  /,  //,  and  the  supra- 


126    GENERAL  PA  THOLOG  Y  AND  TEE  A  TMENT. 

marginal  convolution  produce  paralexia.  These  two  con- 
ditions are  seen  chiefly  in  paralytic  dementia  in  conjunc- 
tion with  defective  speech  (stumbling  over  syllables). 

The  term  di/.sgrap/iia  is  applied  to  disturbances  in  the 
power  of  writing  when  they  are  of  peripheral  origin, 
analogous  to  dysarthria.  They  include  tremulous  writing 
(tremor  senilis,  alcoholicus,  etc.)  and  ataxic  wnting  (heredi- 
tary ataxia,  multiple  sclerosis). 

Dydexia  is  a  functional  disturbance  in  the  power  of 
reading,  with  marked  loss  of  endurance. 

The  presence  of  these  central  disturbances  of  the  speech 
and  other  functions  may  be  determined  in  the  following 
manner  :  The  examiner  engages  the  patient  in  conversa- 
tion, thus  :  He  asks  him,  "How long  have  you  been  ill?'' 
If  the  patient  fails  to  answer,  there  may  be,  after  exclud- 
ing deafness  and  psychosis  : 

(a)  Deaf-mutism. — This  will  be  at  once  recognized  by 
the  patient  beginning  to  gesticulate. 

(h)  Total  motor  and  sensory  aphasia,  which  can  only  be 
determined  by  inquiry  of  a  third  person. 

If  the  patient  nods,  and  answers  other  questions  which 
can  be  answered  by  "  yes ''  or  "  no ''  in  the  same  way,  and 
is  evidently  unable  to  utter  a  word,  it  is  usually  a  sign  of 
motor  aphasia.  If  the  question  makes  no  impression  on 
him  and  he  does  not  comply  w^ith  the  examiner's  request 
to  close  his  eyes  or  perform  other  acts  of  this  nature,  there 
is  sensory  aphasia;  but  if  he  promptly  responds  by  doing 
everything  that  he  is  asked  to  do,  sensory  aphasia  can  be 
excluded  with  certainty. 

If  the  patient  answers  every  question  with  the  same 
word,  such  as  "  no,  no,"  there  is  rnonophasia.  If,  in- 
stead of  answering  correctly,  he  misplaces  his  words, 
syllables,  or  letters,  there  is  paraphasia.  It  is  well  to 
apply  a  rigorous  test  by  asking  the  patient  to  pronounce 
difficult  words  and  phrases,  such  as  "  electricity,"  "  third 
mounted  artillery  brigade,"  and  similar  long  words  or 
phrases.    The  patient  is  then  shown  various  objects,  such  as 


AGRAPHIA.  127 

a  match  or  a  lead-pencil,  and  is  asked  what  they  are  used 
for.  If  he  is  unable  to  indicate  their  use,  either  by  word 
or  gesture,  sensory  aphasia  and  peripheral  visual  dis- 
turbances being  excluded,  there  is  mind-blindness.  If 
the  patient  understands  the  use  of  the  object  but  is  un- 
able to  give  its  right  name  when  asked  to  do  so,  there  is 
optic  aphoMa. 

The  above-mentioned  disturbances  having  been  ex- 
cluded, the  patient  is  now  asked  to  repeat  words,  sentences, 
and  numbers.  If  lie  fails  to  do  this  correctly  because  his 
recollection  of  the  examiner's  words  is  imperfect,  there  is 
amnesic  aphasia. 

The  next  step  in  the  examination  consists  in  testing  the 
power  of  writing.  The  patient  is  asked  to  write  down 
words  and  numbers  from  dictation.  If  he  does  not  write 
at  all,  sensory  aphasia  being  excluded,  there  is  agraphia, 
or  if  he  is  able  to  write  only  one  word,  such  as  "  no,'' 
there  is  monographia.  If  the  writing  is  full  of  mistakes 
and  syllables  and  letters  are  transposed  or  omitted,  there 
is  paragraphia.  If  the  patient  is  unable  to  remember  for 
more  than  an  instant  or  two  what  has  been  dictated,  there  is 
amnesic  agraphia.  In  the  same  way  the  power  of  sponta- 
neous writing  and  copying  should  be  tested,  and  if  the 
patient  is  able  to  write,  he  should  be  examined,  to  deter- 
mine whether  he  understands  what  he  has  written. 

To  test  the  power  of  reading  the  patient  is  asked  to  read 
written  or  printed  words  and  numbers.  If  he  is  unable 
to  do  so,  motor  aphasia  and  visual  disturbances  being  ex- 
cluded, there  is  alexia,  7nonolexia,  or  paralexia.  Again, 
the  examiner  should  note  whether  the  patient  understands 
what  he  reads.  If  there  is  inability  to  remember  for  any 
length  of  time  the  letters  or  numbers  read,  it  is  a  sign  of 
amnesic  alexia.  A  more  rigorous  test  may  be  made  by 
asking  the  patient  to  form  words  and  numbers  from  cer- 
tain given  letters  and  figures. 

2.  Testing  the  Memory. — The  disturbances  of  the 
memory  associated  with  the  power  of  speaking,  reading, 


128    GENERAL  PATHOLOGY  AND  TREATMENT. 

and  writing  have  already  been  described  under  the  head 
of  amnesic  aphasia,  alexia,  and  agraphia. 

In  addition,  the  memory  should  be  tested  in  regard  to 
impressions  acquired  in  early  life  and  to  more  recent 
events,  which  are  obtained  from  the  history. 

The  examination  of  recent  impressions  includes  both 
simple  and  complicated  associations,  single  words  or  num- 
bers, or  rows  of  figures.  Disturbances  of  the  memory  are 
designated  amnesia.  They  occur  in  injuries  to  the  skull, 
contusions,  focal  disease  in  the  brain,  and  in  dementia. 
The  examination  should  include  a  rigorous  test  of  all  the 
various  associations, — auditory,  visual,  tactile,  etc., — the 
details  of  which  can  not  be  given  here. 

3.  Other  Psychic  Disturbances. — The  examiner 
should  determine  w^hether  there  is  any  disturbance  of 
consciousness  (coma,  somnolence,  torpor),  whether  the 
intelligence  is  normal  or  impaired  (dementia,  idiocy), 
whether  there  is  any  morbid  motor  or  sensory  emotional 
condition  (delirium,  emotional  disturbance  with  impaired 
consciousness,  hallucinations,  morbid  sensory  illusions  of 
central  origin,  visions,  morbid  misapprehension  of  sensory 
impressions),  and  whether  there  are  any  delusions  (sys- 
tematized, fixed  or  transient  flight  of  ideas). 

The  presence  of  melancholia  (morbid  depression),  mania 
(morbid  exaltation),  or  hypochondria  must  not  be  over- 
looked. The  finding  of  these  symptoms  does  not  by  any 
means  justify  the  examiner  in  making  a  diagnosis  of  the 
psychosis  of  which  these  symptoms  are  supposed  to  be 
typical. 

Diagnosis. 

The  diagnosis  can  be  made  only  after  a  complete  ex- 
amination and  careful  review  of  the  history.  The  exam- 
iner should  satisfy  himself  in  regard  to  the  following 
questions : 

1.  Is  there  actually  a  disease  of  the  nervous  system,  or  is 
it  merely  simulated  by  anemia,  tuberculosis,  tenia,  etc.  f 


DIAGNOSIS.  129 

2.  Granted  that  there  is  a  nervous  affection,  /.s  it  possible 
that  some  other  bodily  disease  may  be  7'esponsible  for  it 
(arteriosclerosis,  tumors,  diseases  of  the  heart,  lungs,  stomach, 
kidneys,  blood,  etc.,  diabetes)  f 

3.  Is  the  uervous  disease  functional  or  organic  in  char- 
acter f  This  question  can  often  be  answered  at  once,  but 
in  many  cases  it  requires  much  thought  and  a  long  course 
of  observation.  Thus,  choked  disc,  degenerative  muscular 
atrophy  (RD),  loss  of  the  patellar  and  pupillary  reflexes, 
are  always  due  to  an  organic  lesion.  The  mode  of  origin 
of  the  disease  must  be  carefully  considered. 

4-  Granted  that  the  disease  is  organic,  ivhere  is  the  lesion 
situated  f  (See  General  Symptomatology,  Part  IV,  '3.) 
Is  it  a  focal  disease  or  a  system  degeneration  f 

5.  What  is  the  nature  of  the  disease  f  The  answering 
of  this  question  \\\\\  necessitate  a  careful  consideration  of 
the  mode  of  origin  of  the  disease,  its  possible  connection 
with  other  diseases  (infections,  tumors),  the  site  of  the  lesion, 
and  the  bearing  of  other  symptoms  that  may  be  present 
(fever,  cachexia).  In  many  cases  a  single  examination  is 
not  sufficient,  and  not  rarely  the  course  of  the  disease  must 
be  followed  for  some  time  before  a  diagnosis  can  be  arrived 
at.  If,  as  in  many  cases,  a  positive  diagnosis  is  out  of  the 
question,  the  examiner  must  content  himself  w'ith  making 
a  provisional  one.  It  is  well  not  to  make  such  a  diagnosis 
as  paralytic  dementia,  brain-tumor,  or  tabes  dorsalis  with- 
out due  deliberation,  certainly  never  after  the  first  exami- 
nation, without  very  strong  reasons. 

5.   General  Remarks  on  the  Treatment  of  Nervous 
Diseases. 

The  treatment  of  nervous  diseases,  more  than  that  of 
any  other  bodily  affections,  demands  that  the  attending 
physician  should  both  act  and  think  according  to  the  dic- 
tates of  psychology.  Unfortunately,  this  part  of  our  med- 
ical education  still  leaves  much  to  be  desired.     But  it  is 


1 30  GENERA L  PA  THOLOG  Y  A  ND  TREA  TMENT. 

none  the  less  true  that  a  knowledge  of  the  anatomic  and 
clinical  facts  is  far  from  being  all  that  is  required.  The 
treatment  includes  : 

1.  The  Prophylaxis. — No  other  field  of  medicine  pre- 
sents greater  possibiUties  for  the  exercise  of  judgment  in 
forestalling  disaster,  as  there  is  no  other  in  which  so  much 
mischief  is  caused  by  negligence  on  the  part  of  the  attend- 
ing physician.  For  the  guidance  of  the  latter  the  follow- 
ing points  may  be  emphasized.  A  physician  should  with- 
hold his  consent  to  matrimonial  alliances  between  persons 
suffering  from  mental  or  nervous  diseases,  or  between  per- 
sons with  any  inherited  taint  (hereditary  system  diseases). 
The  feeding  and  care  of  children  in  regard  to  proper  hy- 
gienic measures  should  be  under  medical  supervision. 
Patients  should  be  carefully  informed  concerning  the  evil 
effects  of  an  improper  mode  of  life  (alcohol,  tea,  tobacco, 
excesses  of  all  kinds,  morphin,  the  latter  especially  in  the 
case  of  doctors)  and  of  certain  trades  and  professions  (over- 
exertion, working  at  irregular  times,  hygiene  of  factories, 
etc.). 

Careful  directions  should  be  given  in  regard  to  such 
matters  as  personal  cleanliness,  bathing,  clothing,  exercise, 
etc. 

2.  Curative  Treatment. — Unfortunately,  this  is  pos- 
sible in  only  a  few  diseases. 

(a)  Intoxications. — Cases  of  poisoning  by  lead  and 
arsenic  can  be  guarded  against,  or  at  least  very  much 
improved,  by  forbidding  the  patient  to  engage  in  certain 
kinds  of  work  and  by  insisting  on  his  observing  proper 
precautions.  Alcoholism  and  the  morphin  and  cocain 
habits  are  best  treated  in  institutions.  In  almost  every 
case  alcohol,  morphin,  and  cocain  can  be  withdrawn  at 
once.  In  alcoholism  sudden  withdrawal  is  not  followed 
by  any  distinct  symptoms,  in  spite  of  anything  that  may 
have  been  said  to  the  contraiy,  and,  while  it  is  true  that 
sudden  withdrawal  of  cocain  or  morphin  may  produce 
severe  symptoms, — although  these  have  often  been  very 


CURATIVE  TREATMENT.  131 

much  exaggerated, — nev^ertheless,  if  there  is  any  hope  for  a 
patient  at  all,  it  is  not  likely  that  he  will  succumb  to 
them.  Hence  the  so-called  cures  without  coercing  and 
tormenting  the  patient  are  to  be  condemned,  as  they  rarely 
produce  any  permanent  results.  The  practice  of  compen- 
sating the  patient  for  the  loss  of  morphin  by  large  doses 
of  alcohol  is  apt  to  prove  dangerous  in  the  end. 

I  do  not  wish  to  say  that  in  very  severe  cases  morphin 
should  be  withheld  ahogether  during  the  first  three  or  four 
days,  but  it  should  not  be  given  after  that  period,  and 
then  only  when  there  are  unmistakable  objective  signs 
of  collapse. 

(b)  All  syphilitic  cases  where  the  diagnosis  is  abso- 
lutely certain,  and  all  suspected  cases,  should  be  subjected 
as  early  as  possible  to  a  course  of  mercurial  inunctions  (3 
to  5  gm.,  45  grains  to  IJ  drams).  This  may  be  supple- 
mented either  from  the  beginning  or  later  on  by  potassium 
iodid  in  doses  of  forty-five  minims  a  day.  Potassium 
iodid  should  never  be  tried  alone. 

In  malarial  neuralgia  give  quinin  (8  to  24  grains). 

(c)  The  third  class  of  diseases  that  are  amenable  to 
direct  treatment  are  those  which  admit  of  surgical  opera- 
tions. The  num})er  of  these  diseases  has  been  constantly 
growing.  Without  counting  direct  injury  to  the  nerv^ous 
system,  we  have  in  this  category  : 

a.  Brain  diseases  in  which  the  lesion  can  be  accurately 
located  (spicules  of  bone,  purulent  foci),  if  they  are  situ- 
ated near  the  cortex  ;  in  purnlent  foci  exploratory  trephin- 
ing and  puncture  are  perfectly  justifiable. 

In  conditions  of  increased  intracranial  pressure,  such 
as  hydrocephalus,  at  least  a  temporary  improvement  may 
be  eifected  by  trephining  or  paracentesis  of  the  ventric- 
ular system  (the  central  canal  has  even  been,  successfully 
tapped  in  the  lumbar  enlargement ').  Suppurations  due 
to  caries  in  bones  and  joints  exerting  an  injurious  influ- 

^  It  is  to  be  stated,  however,  that  puncture  has  been  followed  by 
sudden  death,  especially  in  cases  of  cerebellar  tumor. 


132  GENERA  L  PA  THOLOG  Y  A  KD  TREA  TMENT. 

ence  on  the  nervous  system  ean,  of  course,  be  reached  by 
surgical  treatment.  Whether  Jacksonian  epilepsy  can 
always  be  successfully  treated  by  surgical  measures  must 
still  be  regarded  as  an  unsettled  question.  In  genuine 
epilepsy  it  is  better  not  to  operate. 

As  regards  tumors,  experience  shows  that  only  very  few 
are  operable ;  but  the  opening  of  brain  abscesses,  on  the 
other  hand,  has  been  followed  by  excellent  results. 

/?.  Diseases  of  the  Spinal  Cord. — Operative  treatment 
has  in  the  past  been  resorted  to  chiefly  in  myelitis  due  to 
compression  by  tumors  or  caries,  and  in  diseases  caused 
by  injury.  The  results,  however,  have  not  been  very 
encouraging.  The  difficulty  of  the  operation  depends  on 
several  factors,  such  as  the  uncertainty  of  the  diagnosis, 
both  as  regards  the  character  of  the  disease  and  its  exact 
localization,  and  the  difficulty  experienced  by  the  surgeon 
in  finding  his  bearings  in  the  operative  field.  Neverthe- 
less, we  may  hope  for  better  results  in  the  future,  especially 
in  cases  which  present  themselves  for  operation  early,  be- 
fore the  graver  irreparable  lesions  in  the  nervous  substance 
have  made  their  appearance  (secondary  degenerations). 

If  secondary  degeneration  has  already  set  in,  all  that 
can  be  hoped  for  is  palliation  of  the  pain. 

y.  Peripheral  Nerves. — The  best  results  have  been  ob- 
tained in  this  portion  of  the  nervous  system,  because  the 
power  of  regeneration  is  far  greater  in  the  nerves  them- 
selves than  in  the  tissues  of  the  brain  and  spinal  cord. 
Complete  repair  is  possible  even  when  some  time  has 
elapsed  after  a  solution  of  continuity  has  taken  place. 
Cicatricial  processes  and  tumors  giving  rise  to  pressure 
symptoms  have  always  been  treated  by  operative  means 
and  with  very  good  success. 

The  repair  of  a  nerve  that  has  been  divided  in  its  con- 
tinuity can  often  be  hastened  by  means  of  a  plastic  op- 
eration. The  success  of  a  surgical  operation,  as  has  been 
said,  depends  chiefly  on  an  early  and  exact  localization  of 
the  lesion. 


SYMPTOMATIC  TREATMENT.  133 

3.  In  regard  to  the  many  successful  operations  for  the 
transplantation  of  tendons  to  healthy  muscles,  consult  the 
paragraph  on  Anterior  Poliomyelitis. 

3.  Symptomatic  Treatment. — This  will  be  entirely 
successful  in  all  cases  in  wliich  no  grave  degenerative 
process  has  made  its  appearance.  With  the  present  means 
at  our  command  the  prognosis  is  quite  unfavorable  in 
degenerative  aifections  of  the  cell,  fiber,  and  muscle,  espe- 
cially when  they  are  of  central  origin.  Individual  symp- 
toms can  sometimes  be  treated  and  may  even  be  tempo- 
rarily improved. 

(a)  Psychic  Treatment  (Moral  Treatment). — Much 
may  be  accomplished  by  judicious  encouragement,  by 
rational  explanation,  and  by  showing  the  patient  that  he 
is  alarming  himself  unnecessarily ;  a  certain  dictatorial 
severity  even  may  be  of  great  service.  The  importance 
of  some  systematic  occupation  should  be  emphasized. 
Thus,  a  schedule  of  hours  may  be  suggested  for  the  day's 
work,  and  the  patient  may  be  encouraged  to  engage  in  out- 
door occupations,  such  as  horticulture,  etc.  This  can 
not  be  insisted  on  too  strongly,  especially  in  the  case  of 
neuroses. 

It  is  of  the  highest  importance  that  the  physician  should 
have  the  patient's  entire  confidence,  and  the  best  way  to 
obtain  this  is  by  accurate  examination  and  careful  diag- 
nosis. A  careful  examination  in  itself  often  has  a  decided 
moral  effect,  and  may  be  said  to  be  one  of  the  most 
important  therapeutic  measures. 

Hypnotism  should  be  resorted  to  only  in  cases  which 
ought  to  be  treated  by  psychic  means  and  in  which  the 
above-mentioned  measures  have  failed.  There  is  no  doubt 
that  the  treatment  is  often  effective,  but  in  many  cases  the 
results  are  not  permanent  and  in  not  a  few  the  ultimate 
effect  is  even  harmful.  No  one  who  does  not  possess 
special  qualifications  and  is  not  perfectly  familiar  with 
all  the  details  of  hypnotism  has  any  right  to  resort  to  this 


134  GENERAL  PATHOLOGY  AND  TKEATMEEIT. 

mode  of  treatment.  (For  particulars  in  this  respect  con- 
sult the  paragraph  on  Hysteria.) 

(b)  Physical  (Hygienic)  Treatment. — The  diet,  the 
hours  of  sleep  and  rest,  and  other  matters  of  that  kind 
should  be  regulated  according  to  general  therapeutic  prin- 
ciples. If  possible,  all  artificial  measures  should  be  dis- 
pensed with.  The  use  of  alcoholic  beverages  should  be 
restricted  or,  better,  forbidden  altogether,  and  the  physi- 
cian should  do  everything  in  his  power  to  combat  the 
senseless  doctrine  of  the  nerve-strengthening  power  of 
wine,  which  is  still  held  by  the  laity  and  by  many  apoth- 
ecaries and  physicians.  Fruit,  cocoa,  tea,  mild  coffee, 
even  cider  and  beer  in  moderation,  may  be  recommended. 

Hydrotherapy. — Sponging  with  moderately  cold  water, 
douches,  cool  (77°  to  86°  F.)  and  warm  (90°  to  100°  F.) 
baths,  hot  and  cold  packs,  and  hot-water  compresses  may 
be  employed.  After  a  w^arm  bath  the  patient  should 
always  be  sponged  with  cold  water. 

It  is  often  very  advantageous  to  send  the  patient  to  the 
various  baths,  especially  the  smaller  places,  or  to  the  sea- 
shore or  the  mountains. 

Massage,  gymnastiG  exercise,  and  Weir  MitcheWs  treat- 
ment ("  Mastkuren^')  are  often  useful  if  carried  out  accord- 
ing to  the  physician\s  orders. 

Electricity  is  often  the  last  resort.  The  question  as  to 
how  it  acts,  whether  indirectly,  by  psychic  impression,  or 
directly,  is  still  a  matter  of  dispute.  Both  the  galvanic 
and  the  farad ic  currents  are  used.  According  to  the  gen- 
eral opinion,  the  galvanic  current  acts  on  deeper  structures 
than  does  the  faradic.  The  galvanic  current  is  to  be  em- 
ployed in  painful  affections  and  in  affections  of  central 
origin ;  the  anode  has  a  quieting  effect,  while  the  cathode 
is  irritating ;  hence  the  anode  should  be  applied  to  the 
painful  spot.  The  faradic  current  is  indicated  in  periph- 
eral diseases,  especially  in  muscular  paralyses.  As  it  is 
very  important  not  to   have  the  current  too  strong,  the 


MEDICINAL  TREATMENT.  135 

instrument  .should  always  be  provided  with  a  galvan- 
ometer. 

(c)  Medicinal  Treatment. — This  should  not  be  the 
first,  but  the  last,  remedy  to  be  tried,  unless  there  are 
special  indications.  The  ruling  principle  should  always 
be  nil  nocerc,  for  in  any  case  drugs  are  of  little  value,  and 
the  risk  is  great  in  proportion  to  the  possible  benefit. 
Hence  the  patient  should  not  be  subjected  to  unnecessar}' 
expense.  There  are  certain  drugs,  however,  which  unques- 
tionably influence  the  nutrition,  such  as  arsenic  (arsenious 
acid,  Y^y  to  i  grain  ;  Fowler's  solution,  5  to  10  drops  a 
day ;  iron,  Blaud's  pills  ;  iron  and  quinin  ;  iron  and  arsenic 
pills). 

As  sedatives,  the  bromids  are  to  be  recommended  (the 
potassium,  sodium,  or  ammonium  bromid,  or  combinations 
of  them,  1  to  4  drams  a  day).  Antipyrin  may  also  be 
given,  15  to  30  grains,  etc.  To  allay  the  pain,  such 
remedies  as  opium,  morphin  (contraindicated  in  neurosis), 
codein,  and  heroin  are  found  indispensable.  In  neuralgia 
the  following  remedies  have  been  recommended  :  Anti- 
pyrin, 15  to  30  grains  ;  quinin,  8  to  24  grains  ;  the  salicyl- 
ates (sodium  salicylate,  45  grains  to  3  drams ;  salicylic 
acid,  Y  to  1  dram) ;  phenacetin,  8  to  24  grains ;  antinervin, 
8  to  24  grains;  salophen,  8  to  24  grains;  analgen,  15  to 
30  grains;  salipyrin,  15  to  24  grains;  pyramidon,  8 
grains,  etc. 

The  following  hypnotics  are  the  most  commonly  used  : 
Sulphonal,  15  to  30  grains;  hypnal,  8  to  30  grains;  tri- 
onal,  8  to  24  grains  ;  chloral,  15  to  30  grains  ;  and  chloral- 
amid,  30  to  45  grains.  Other  remedies  are  often  employed 
on  theoretic  grounds  ;  they  are  :  Ergotin,  ^  to  4J  grains  ; 
silver  nitrate,  ^  to  ^  grain  ;  strychnin,  -gJ^  to  -^^  grain  ; 
atropin,  yi^  to  -^-^  grain  per  diem  ;  etc.  Some  of  these 
are  very  dangerous  poisons  and  should  be  used  guardedly, 
as  their  value  in  any  case  is  very  doubtful.  Ointments 
and  cutaneous  irritants  often  have  a  good  sedative  effect. 


PART  V. 

SPECIAL    PATHOLOGY    AND    TREAT- 
MENT. 

(Plates  75  to  84  and  preceding  Plates.) 


1.  DISEASES  OF  THE  MEMBRANES  AND   BLOOD- 
VESSELS  OF   THE    BRAIN. 

On  the  surface  of  the  brain,  diseases  of  these  structures 
act  on  the  cortical  substance ;  at  the  base  of  the  brain,  on 
the  cranial  nerves  at  their  point  of  exit ;  in  the  spinal  cord, 
on  the  nerve-roots — the  symptoms  being  thus  dependent 
on  the  seat  of  the  morbid  process. 

L   Internal  Hemorrhagic   Pachymeningitis  (Hema- 
toma of  the  Dura  Mater). 

Morbid  Anatomy. — An  inflammatory  membranous  ex- 
udate forms  on  the  inner  surface  of  the  dura,  with  devel- 
opment (secondary?)  of  interstitial  hemorrhages.  The 
cause  is  unknown. 

The  disease  occurs  in  adults  in  association  with  alco- 
holism, senility,  or  paralytic  dementia,  and  may  be  idio- 
pathic. 

The  symptoms,  which  come  on  successively  as  the 
hemorrhages  develop,  consist  of  headache  and  irritative 
and  paralytic  cortical  phenomena  (convulsions  limited  to 
one  side  of  the  body,  hemiplegia,  fever). 

The  diagnosis  must  be  made  from  brain-tumor,  which 
is  steadily  progressive  ;  cerebral  hemorrhage,  which  rarely 
gives  rise  to  irritative  symptoms ;   meningitis  (different 

136 


EPIDE3IIC  CEREBROSPINAL  MENINGITIS.  137 

course  and  the  presence  of  symptoms  referable  to  the 
base);  uremic  coma  (examination  of  urine,  course);  and 
cerebral  syphilis  (concomitant  symptoms). 

Treatment. — Rest,  ice-bag,  venesection,  calomel  (gr.  iv, 
t.  i.  d.),  drastics,  and  relief  of  symptoms  as  they  arise 
(hypnotics  and  morphin). 

2.  Acute  Leptomeningitis  (Meningitis  of  the  Con- 
vex Surface). — (a)  Epidemic  Cerebrospinal  Meningitis. 
— An  epidemic  infectious  disease,  occurring  also  sporadi- 
cally, caused  by  the  di])lococcus  intracellularis. 

Morbid  Anatomy. — The  presence  and  development  of 
the  diplococcus  (which  enters  through  the  nose,  through 
excoriations,  or  through  the  lymphatic  and  vascular  chan- 
nels (?) )  set  up  an  inflammation  in  the  soft  membranes  of 
the  spinal  cord.  The  meshes  of  the  pia,  especially  on  the 
convex  surface  of  the  cerebral  hemispheres,  become  filled 
with  an  exudate,  at  first  serous  and  later  purulent. 

Course. — The  onset  of  the  disease  is  quite  abrupt ;  it 
occurs  most  frequently  in  young  individuals,  and  begins 
with  a  general  feeling  of  malaise,  followed  by  violent  head- 
ache, vomiting  (cerebral),  and  chills.  The  condition  rap- 
idly becomes  worse.  Herpes  labialis,  persistent  high  tem- 
perature, and  marked  leukocytosis  are  characteristic.  The 
occurrence  of  rigor  and  pains  in  the  muscles  of  the  neck 
on  movement  of  the  head  (irritation  of  the  upper  cervical 
roots)  and  clouding  of  the  consciousness  practically  deter- 
mine the  diagnosis.  Later  on  there  are  delirium  and 
symptoms  of  cortical  irritation  (convulsions,  palsies,  mono- 
plegia and  hemiplegia,  and  hyperesthesia) ;  finally,  coma, 
trismus,  opisthotonos,  retention  of  urine  and  feces,  and 
Cheyne-Stokes  breathing.  In  the  severest  cases  death 
occurs  before  the  eighth  day  (meningitis  siderans)  :  moder- 
ately severe  cases  may  be  protracted  to  eight  weeks  and 
longer,  although  recovery  is  possible  even  when  the  disease 
is  very  severe. 

Sequelae.  —  Deafness  (lesion  of  the  auditory  nerve), 
blindness,  cephalalgia,  paralyses,  brain  abscess. 


138  SPECIAL  PATHOLOGY  AND  TBEATMENT. 

The  diagnosis  must  be  made  from  typhus  (gradual 
onset,  absence  of  herpes,  and  leukocytosis),  pneumonia 
(sputum,  pulmonary  symptoms),  pyemia  (purulent  foci, 
absence  of  rigidity  of  the  neck),  tubercular  meningitis 
(basal  symptoms,  signs  of  constitutional  tuberculosis),  puru- 
lent meningitis  (primary  purulent  focus),  and  ulcerative 
endocarditis  (not  epidemic). 

Treatment. — Rest ;  cold  packs  ;  baths  are  too  severe, 
although  warm  baths  have  lately  been  much  lauded  ;  ice- 
bag  ;  leeching  (mastoid  process) ;  calomel  (four  grains  twice 
repeated) ;  blister  to  the  occiput ;  inunctions  with  blue 
ointment ;  antipyretics ;  narcotics. 

(b)  Purulent  Meningitis. — This  follows  suppurative 
processes  in  the  ear  (otitis  media,  caries  of  the  petrous 
portion  of  the  temporal  bone),  erysipelas,  pyemia,  and 
other  acute  infectious  diseases.  Accordingly,  various 
micro-organisms  are  found  :  streptococcus  pyogenes,  strep- 
tococcus erysipelatis,  staphylococcus  aureus  and  albus. 

The  morbid  anatomy  is  the  same  as  in  the  foregoing 
variety.  The  most  extensive  purulent  foci  are  found  on 
the  convex  surface,  but  may  also  occur  elsewhere. 

Course. — The  onset  and  course  are  the  same  as  in  the 
foregoing  variety.  There  is,  perhapsj  a  somewhat  greater 
liability  to  paralysis  of  the  cranial  nerves  that  make 
their  exit  at  the  base  of  the  brain ;  optic  neuritis  and 
pupillary  changes  occur. 

For  diagnosis  see  under  (a).  It  is  particularly  import 
tant  to  determine  the  original  cause  of  the  disease. 

Treatment  as  under  (a).     Surgical  interference. 

3,  Tubercular  Meningitis  (Basilar  Meningitis). — 
It  follows  primary  tuberculosis  of  the  lungs,  lymphatic 
glands,  or  bones,  particularly  in  children. 

Morbid  Anatomy. — The  tubercle  bacilli  are  carried  by 
the  circulation  to  the  soft  membranes ;  here  they  lead  to 
the  formation  of  miliary  tubercles  and  the  deposition  of  a 
fibrinous,  gelatinous  exudate  on  the  base  of  the  brain,  in 
the  meshes  of  which  are  imbedded  miliary  nodules.     The 


BRAIN  SYPHILIS.  139 

nodules  may  spread  to  the  brain  substance  and  form 
tumor-like  solitary  tubercles. 

Course. — The  disease  begins  gradually,  with  malaise, 
headache,  and  vomiting.  After  a  time  the  symptoms  of 
cortical  irritation  become  more  marked,  with  delirium 
and  convulsions  (cri  hydrence})lia]ique  in  children),  tris- 
mus, and  irregular  heart  action.  There  are  somnolence, 
temperature  up  to  102.2°  F.,  irregular  fever,  rigidity  of 
the  neck,  coma. 

Later,  paralysis  of  individual  cranial  (oculomotor,  facial, 
abducens)  nerves,  monoplegia,  aphasia,  death. 

Diagnosis. — The  disease  must  be  diflPerentiated  from 
purulent  meningitis,  q.  v.  Diagnosis  is  confirmed  by  find- 
ing tubercle  bacilli  in  the  sputum  or  in  the  cerebrospinal 
fluid  withdrawn  by  lumbar  puncture. 

Tubercles  on  the  choroid. 

Treatment  as  under  2. 

4.  Syphilitic  or  Gummatous  Meningitis  and  Brain 
Syphilis. — It  makes  its  appearance  in  the  secondary  and 
tertiary  periods  of  syphilis,  never  until  several  months 
after  the  infection.  The  characteristic  syphilitic  neoplasms 
(gumma,  infiltration,  caseation)  make  their  appearance  in 
the  soft  membranes,  especially  on  the  base  of  the  skull, 
and  in  close  relation  with  the  blood-vessels  in  that  region. 
Three  forms  of  brain  syphilis  are  distinguished  : 

(a)  The  true  diffuse,  basilar  syphilitic  meningitis, 
characterized  by  the  formation  of  thickened  plates,  in  some 
cases  circumscribed  to  definite  localities.  The  symptoms 
are  in  the  main  the  same  as  those  of  tubercular  basal 
meningitis. 

(6)  Formation  of  isolated  gummata  in  the  membranes, 
rarely  in  the  substance  of  the  brain.  The  symptoms  are 
those  of  brain-tumor. 

(c)  A  form  associated  with  peculiar  alterations  in  the 
blood=vessels  (syphilitic  endarteritis),  with  or  without 
diffuse  or  circumscribed  gummatous  meningitis.  The 
intima  of  the  vessels  at  the  base  of  the  brain  undergoes 


140  SPECIAL  PATHOLOGY  AND  TREATMENT. 

proliferation,  so  that  the  lumen  is  narrowed.  This  is  apt 
to  be  followed  by  thrombosis  and  resulting  necrosis.  (See 
Embolism.)  The  individual  varieties  often  occur  in  com- 
bination, so  that  the  clinical  picture  of  brain  syphilis  pre- 
sents numerous  variations.  The  symptoms  vary  much  in 
intensity,  exacerbations  alternating  with  temporary  remis- 
sions. 

Course. — The  disease  begins  with  meningitic  symptoms 
(headache,  vomiting),  which  are  followed  by  attacks  of 
partial  unconsciousness,  palsies  in  the  extremities,  convo- 
lutions, dementia,  and  apathy,  together  with  lesions  of  the 
basal  nerves  (optic  atrophy  and  neuritis,  oculomotor,  facial 
paralysis,  etc.)  ;  polyuria  and  polydipsia  occur.  The  soft- 
ening process  gives  rise  to  successive  attacks  of  hemiplegia, 
and  the  picture  is  further  complicated  by  aphasia  and  epi- 
leptic seizures.  Recovery  is  possible,  but  more  or  less 
paralysis  usually  remains. 

Diagnosis. — The  signs  of  a  former  infection  play  the 
most  important  part  in  the  diagnosis  (abortions,  scars, 
glandular  enlargement)  ;  in  doubtful  cases  the  diagnosis 
may  later  be  reached  ex  jvvantibus.  Syphilis  should  be 
thought  of  in  any  case  of  meningitis  which  presents  an 
unusual  course. 

Treatment. — Inunctions,  potassium  iodid  (see  Gen- 
eral Treatment) ;  symptomatic. 

5.  Thrombosis  of  the  Sinuses. — Thrombosis  in  the 
venous  sinuses  is  usually  secondary  to  other  disease  local- 
ized in  their  immediate  neighborhood,  especially  if  of  an 
inflammatory  character,  the  process  extending  to  the  wall 
of  the  sinus  (phlebitis).  It  may  occur  in  caries  and  osteo- 
myelitis of  the  petrous  portion  of  the  temporal  bone  and 
mastoid  process,  in  purulent  meningitis,  brain  abscess, 
phlegmon  ;  or  spontaneously,  in  old  age  (marantic  throm- 
bosis, chlorosis,  cachexia). 

Marantic  thrombosis  is  frequently  localized  in  the  supe- 
rior longitudinal  and  in  the  transverse  sinuses.  In  aural 
affections  the  thrombosis  commonlv  forms  in  the  transverse 


THROMBOSIS.  141 

sinus.  The  thrombus  breaks  (U)wn  as  the  result  of  secon- 
dary infection  and  leads  to  metastatic  pyemia,  the  emboli 
making  their  way  through  the  jugular  vein  and  right  heart 
into  the  lung. 

The  symptoms  vary  according  to  the  seat  of  the  throm- 
bus. Meningitic  symptoms  (headache,  vomiting,  convul- 
sions, coma)  are  usually  present ;  also  paralysis  and  rigor 
of  the  muscles  of  the  neck.  Thrombosis  of  the  transverse 
sinus  produces  edema  over  the  mastoid  ])rocess  (venous 
stasis).  The  internal  jugular  vein  on  the  same  side  is 
flaccid,  and  the  external  jugular  vein  empties  itself  more 
rapidly.  In  thrombosis  of  the  cavernous  sinus  the  oph- 
thalmic veins  are  engorged,  the  lids  are  edematous,  the 
conjunctivae  are  chemotic  ;  protrusion  of  the  eyeball  and 
ocular  palsies  are  present  (the  oculomotor  and  abducens 
occupy  compartments  in  the  wall  of  the  sinus).  Throm- 
bosis of  the  superior  longitudinal  sinus  betrays  itself  by 
venous  stasis  in  the  veins  of  the  nose  (epistaxis). 

A  positive  diagnosis  is  not  always  possible,  because 
the  condition  is  often  masked  by  the  symptoms  of  the 
primary  disease  (abscess,  meningitis).  It  can  be  made 
with  certainty  only  after  the  above-mentioned  hypostatic 
phenomena  have  made  their  appearance. 

Treatment. — Either  surgical  (opening  of  the  sinus  and 
packing  with  gauze)  or  symptomatic. 

6.  For  diseases  of  the  arteries  and  their  consequences 
see  Hemorrhage,  P^mbolism  and  Aneurysm  in  the  follow- 
ing section. 

II.  THE    DISEASES   OF   THE    BRAIN   SUBSTANCE. 

A.  ORGANIC  DISEASES. 

I.  Circulatory  Disturbances  and  their  Consequences. 

(a)  Anemia  and  Hyperemia. — These  two  conditions 
occur  as  temporary  or  lasting  symptoms  in  a  great  number 
of  conditions,  as  in  exhaustion,  fever,  and  the  various 
forms  of  anemia. 


142  SPECIAL  PATHOLOGY  AND  TREATMENT. 

Temporary  cerebral  (especially  cortical)  anemia  gives 
rise  to  attacks  of  syncope.  Persistent  anemia  after  hem- 
orrhages or  in  secondary  and  primary  anemia  due  to 
other  causes  shows  itself  in  impairment  of  the  general 
condition,  sonniolence,  fatigue,  tinnitus  aurium,  vertigo, 
nausea,  and  fits  of  yawning. 

Treatment. — Infusion  of  salt  solution  ;  horizontal  posi- 
tion ;  enemata ;  cutaneous  irritation  in  acute  anemia ; 
rubefacients  ;  ^gg  and  milk  diet ;  iron  and  arsenic  and 
other  symptomatic  remedies  in  chronic  anemia.  Alcohol 
in  the  form  of  red  wine  is  quite  superfluous  and  rather  in- 
jurious than  beneficial  in  the  treatment  of  anemia. 

Hyperemic  conditions,  such  as  sudden  attacks  of  heat, 
palpitation,  vertigo,  a  feeling  of  oppression  in  the  head, 
occur  in  plethoric  individuals  and  those  of  the  so-called 
epileptic  habit.  It  is  probable  that  arteriosclerosis  is 
largely  responsible  for  these  symptoms,  although  this  is 
difficult  to  demonstrate. 

Treatment. — Regulation  of  the  diet ;  restriction  in  the 
use  of  alcohol  and  tobacco  ;  baths  (Marienbad)  ;  exercise, 
and  regulation  of  the  cardiac  and  renal  functions. 

(b)  Cerebral  Hemorrhage. — The  arteries  of  the  brain 
are  characterized  by  an  unusual  tendency  to  the  formation 
of  miliary  and  larger  aneurysms,  rupture  of  which  is  re- 
sponsible for  a  great  variety  of  cerebral  lesions.  The 
bursting  of  even  a  very  small  aneurysm  may  lead  to  the 
gravest  consequences  if  an  important  pathway  or  nerve 
center  is  destroyed  by  the  hemorrhage.  Miliary  aneurysms 
of  this  character  may  occur  in  any  arteries  of  the  brain, 
but  are  found  most  frequently  in  the  branches  of  the  artery 
of  the  fissure  of  Sylvius,  the  most  important  branch  of 
which,  the  lenticulostriate  artery  (shown  in  Fig.  5,  p.  20), 
is  involved  more  often  than  any  other.  The  resulting  ex- 
travasation of  blood  produces  more  or  less  extensive  de- 
struction of  the  surrounding  brain  substance.  If  a  throm- 
bus is  formed,  the  hemorrhage  becomes  arrested  and  the  ex- 
travasated  blood  is  absorbed  and  partly  converted  into  con- 


CEREBRAL  HEMORRHAGE.  143 

nective  tissue.  On  the  surface  of  the  brain  this  process 
leaves  a  defect,  while  in  the  interior  a  cyst  remains  at  the 
site  of  the  hemorrhage. 

The  causes  that  may  lead  to  the  formation  of  such  an 
aneurysm  are  arteriosclerosis  due  to  chronic  alcoholism, 
syphilis,  gout,  chronic  nephritis,  old  age,  and  other  un- 
known causes. 

A  hemorrhage  occurring  in  the  region  of  the  basal 
ganglia  and  adjacent  portions  of  white  matter — the  inter- 
nal capsule — is  followed  by  the  gravest  consequences. 
This  region  is  supplied  principally  by  the  above-mentioned 
branch  of  the  artery  of  the  fissure  of  Sylvius,  which,  from 
its  great  liability  to  hemorrhage,  has  been  named  by  Char- 
cot the  "  artere  d  ^hemorrhagie.^' 

The  hemorrhage  is  attended  by  the  phenomena  of  cere- 
bral apoplexy,  the  so-called  apoplectic  stroke.  After  the 
phenomena  of  the  initial  injury  have  run  their  course, 
a  permanent  hemiplegia  remains  as  a  residuum.  The 
occurrence  of  an  apoplexy  may  be  preceded  by  certain  pro- 
dromal symptoms  affecting  the  circulation,  such  as  head- 
ache, vertigo,  tinnitus  aurium,  and  fatigue  on  the  slightest 
exertion.  In  many  cases,  however,  the  apoplectic  stroke 
occurs  without  any  warning  and  without  any  ascertainable 
cause,  or  it  may  come  on  suddenly  after  bodily  exertion 
or  mental  excitement.  The  patient  is  suddenly  seized 
with  nausea,  his  head  swims,  he  becomes  confused  and 
falls  to  the  ground  unconscious.  This  is  known  as  the 
insult.  It  may  last  only  a  few  minutes  or  several  days, 
depending  on  the  severity  of  the  case. 

During  the  period  of  insult  the  patient  remains  in  a 
state  of  complete  unconsciousness  and  fails  to  react  to 
stimuli.  The  respiration  is  slow  and  stertorous  (snoring), 
often  intermittent,  pupillary  reaction  is  uncertain,  the  ex- 
tremities are  motionless,  and  when  the  arm  is  released,  it 
falls  lifeless  by  the  patients  side.  In  some  cases  mild 
spastic  phenomena  are  observed.  There  is  retention  of 
the  urine  and  feces,  and  sometimes  conjugate  deviation  of 


144  SPECIAL  PATHOLOGY  AND  TREATMENT. 

the  eyeballs.  The  temperature  may  be  subnormal  or 
normal,  or  hyperpyrexia  may  even  be  present,  especially 
toward  the  end.  If  death  does  not  occur  during  this 
period, — and  this  will  depend  on  the  extent  and  location 
of  the  injury, — the  patient  gradually  recovers  from  his 
stupor,  regains  consciousness,  and  the  exact  nature  of  the 
paralysis  is  now  first  discovered. 

The  paralysis  is  usually  much  more  extensive  imme- 
diately after  the  hemorrhage,  and  the  condition  gradually 
improves  more  or  less  in  the  course  of  a  few  weeks. 
The  initial  symptoms,  which  tend  to  disappear  partially 
during  the  first  weeks,  are  known  as  indirect  focal  symp- 
toms. They  depend  on  the  pressure  exerted  by  the  dis- 
eased focus  on  neighboring  portions,  and  therefore  dis- 
appear when  the  corresponding  regions  of  the  brain  recover 
themselves. 

The  direct  focal  symptomSy  on  the  contrary,  are  irre- 
mediable and  permanent,  as  they  are  due  to  the  destruction 
of  definite  nerve  paths  and  centers.  They  vary  greatly 
with  the  localization  and  extent  of  the  hemorrhage, 
ranging  from  slight  transient  (passagere)  hemiparesis  to 
total  hemiplegia,  with  hemianesthesia  and  hemianopsia. 
The  muscular  paralysis  in  cerebral  hemorrhages  usually 
affects  an  entire  muscle  mechanism — that  is,  a  group  of 
muscles  functionally  associated.  If  the  hemorrhage  is 
located  in  the  left  hemisphere,  it  follows  that  the  paralysis 
will  in  most  cases  be  accompanied  by  some  form  of  aphasia. 
Hemorrhages  in  the  white  matter  may  exist  without  pro- 
ducing any  symptoms,  while  a  hemorrhage  in  the  brain- 
stem may  produce  crossed  hemiplegia.  (Consult  Part 
IV,  3.) 

The  affected  muscles  show  spastic  paralysis,  with  a  ten- 
dency to  the  formation  of  contractures,  but  without  degen- 
erative atrophy.  The  tendon  reflexes  are  exaggerated  ; 
the  cutaneous  reflexes  on  the  paralyzed  side  are  frequently 
diminished  (see  p.  82).  In  rare  cases  a  form  of  atrophy 
developing  with  unusual  rapidity  has  been  observed  (lesion 


EMBOLISM.  145 

of  the  optic  thalamus  ?);  cerebral  atrophy.  The  hemiplegic 
gait  has  been  referred  to  on  page  108.  The  following 
movements  are  often  permanently  lost :  opening  of  the 
hand  and  supination  of  the  arm,  while  the  power  of  closing 
the  hand  and  pronating  the  arm  is  often  retained. 

Choreic  and  athetoid  irritative  phenomena  may  occur  on 
the  side  of  the  hemiplegia  (posthemiplegic  hemichorea, 
hemiathetosis).  In  extensive  or  in  repeated  hemorrhages 
(which  are  quite  common),  the  intelligence  of  the  indi- 
vidual suffers ;  he  becomes  morbidly  irritable  or  total 
dementia  may  develop  secondarily. 

Diagnosis. — Cerebral  hemorrhage  is  to  be  differentiated 
from  uremic  coma  (urine),  diabetic  coma  (acetone  odor, 
sugar),  extrameningeal  hemorrhage  from  the  middle  menin- 
geal artery  in  fracture  of  the  skull  (history,  typical  course 
of  the  increasing  brain  pressure),  cerebral  embolus  (early 
age,  heart  diseases,  symptoms  less  severe,  pachymeningitis, 
q.  v.).     (For  the  topical  diagnosis  consult  Part  IV,  3,  I.) 

Treatment. — Prophylaxis.  (See  under  Hyperemia.) 
During  the  period  of  insult  ice-bag,  rest,  evacuation  of  the 
bladder  and  rectum,  venesection,  stimulants.  After  the 
period  of  insult  reassurance  of  the  patient,  gymnastic 
exercise,  electricity,  massage,  baths  (salt  and  mud) ;  symp- 
tomatic. 

(c)  Brain  Embolism  and  Thrombosis. — Embolism  oc- 
curs when  fibrin  clots  are  swept  into  the  arteries  of  the 
brain  and  lodge  in  one  of  the  smaller  branches.  The  em- 
bolism is  usually  derived  from  the  left  heart  (endocarditis 
of  the  mitral  valve  or  of  the  aorta).  It  traverses  the 
internal  carotid  and  becomes  arrested  in  a  vessel  of  the 
first,  second,  or  third  order,  according  to  its  size,  fre- 
quently in  the  artery  of  the  fissure  of  Sylvius  on  the  left 
side.  As  the  arteries  of  the  brain  are  end  arteries  and 
the  collateral  circulation  can  not,  therefore,  be  reestab- 
lished, the  area  supplied  by  the  occluded  v^essel  undergoes 
necrosis.  Softening  takes  place  (see  under  General  Pa- 
thology), the  contents  of  the  softening  focus  are  absorbed, 
10 


146  SPECIAL  PA  THOLOG  Y  A  ND  TEE  A  TMENT. 

and  a  defect  (yellow  plate)  remains  at  the  site  of  the 
lesion  if  situated  on  the  surface,  or  a  cyst  if  the  necrotic 
area  was  in  the  substance  of  the  brain. 

Sometimes  occlusion  of  the  vessels  and  its  consequences 
may  occur  by  primary  thrombus  formation  in  the  brain 
arteries,  without  any  embolic  process  having  taken  place 
(syphilitic  obliterating  endarteritis,  arteriosclerosis).  Foci 
of  softening  are  often  multiple. 

Course. — The  clinical  symptoms  vary  according  to  the 
individual  artery  occluded  ;  in  the  main  they  are  the  same 
as  in  cerebral  hemorrhage. 

Symptoms. — Embolism  produces  a  primary  apoplectic 
insult  similar  to  that  observed  after  hemorrhage,  but  the 
coma  does  not  last  so  long  and  is  not  so  deep  as  in  the 
former  condition.  On  the  other  hand,  prodromal  symp- 
toms may  be  more  numerous  and  more  marked  in  em- 
bolism, and  especially  in  primary  thrombus  formation. 
There  is  the  same  appearance  of  direct  and  indirect  focal 
symptoms,  but  the  indirect  symptoms  disappear  more  rap- 
idly, as  some  anastomosis  always  takes  place  at  the  boun- 
dary of  the  necrotic  area.  Symptoms  that  fail  to  disap- 
pear after  a  few  days  are  irremediable  and  persist  perma- 
nently as  direct  focal  symptoms.  According  to  the  seat 
of  the  embolus,  there  may  be  rapidly  disappearing  hemi- 
paresis,  and  lasting  and  more  or  less  extensive  hemiplegia  ; 
aphasia  is  more  frequent  than  in  hemorrhage ;  alternating 
palsies,  hemianopsia,  etc.,  occur. 

For  diagnosis  and  treatment  see  under  Hemorrhage. 

(d)  Aneurysms. — The  larger  aneurysms  occur  most 
frequently  in  the  arteries  at  the  base  of  the  brain,  the 
artery  of  the  fissure  of  Sylvius,  carotid,  anterior  commu- 
nicating artery,  basilar  and  vertebral  arteries.  Owing  to 
the  pressure  on  the  brain  substance,  cranial  nerves,  and 
pyramidal  tract  in  the  pons  and  medulla  oblongata,  alter- 
nating hemiplegias  make  their  appearance.  Aneurysm 
of  the  internal  carotid  gives  rise  to  pulsating  exophthal- 
mos. 


BRA  IN  A  BSCESS.  1 4  7 

(e)  Arteriosclerosis  of  the  Arteries  of  the  Brain. 
— The  symptoms,  in  addition  to  a  tendency  to  hemor- 
rhage, thrombosis  (softening  foci  and  aneurysm),  are  such 
as  have  been  mentioned  under  Cerebral  Hyperemia : 
milder  grades  of  hemiparesis,  transient  attacks  of  vertigo, 
visual  disturbances,  etc.,  depending  on  various  circulatory 
disturbances. 

For  the  treatment  see  under  Hyperemia. 

2.  Inflammatory  Diseases  of  the  Brain -Substance. 

(a)  Brain  Abscess.— This  occurs  after  injury  to  the 
skull  or  in  connection  with  other  inflammatory  processes, 
such  as  purulent  meningitis,  caries,  otitis  media,  osteomye- 
litis, pyemia,  and  abscess  of  the  lungs.  An  abscess  is 
called  idiopathic  when  no  primary  affection  can  be  discov- 
ered. 

Abscesses  are  most  frequently  found  in  the  temporal 
lobe  and  in  the  cerebellum,  especially  when  they  are  sec- 
ondary to  disease  of  the  ear. 

The  following  organisms  have  been  found :  Staphy- 
lococcus aureus  ;  the  diplococcus  of  Frtinkel  ;  strepto- 
coccus pyogenes ;  oidium  albicans  ;  tubercle  bacilli  ; 
bacillus  proteus,  and  others. 

Course. — A  brain  abscess  may  become  encapsulated  and 
thus  remain  latent  for  a  long  period  (as  long  as  ten  years 
in  some  cases),  and  then,  without  any  discoverable  cause, 
suddenly  produce  violent  focal  symptoms  complicated  by 
symptoms  of  meningitis  (rupture  into  a  ventricle  from 
without). 

The  symptoms  of  brain  abscess  are  partly  paralytic 
(the  focal  symptoms)  and  partly  irritative.  (1)  General 
symptoiiu^ :  Persistent,  dull  headache  ;  vomiting  ;  vertigo  ; 
irregular  low  fever  ;  at  times  comatose  conditions  ;  retard- 
ation of  the  pulse-rate  and  convulsions.  (^)  Focal  symp- 
toms, including  a  great  variety  of  paralytic  and  irritative 
phenomena,  as  hemiplegia,  heniituiopsia,  epileptic  attacks ; 
in  cerebellar  abscess,  cerebellar  ataxia ;  w^hen  the  abscess 


148  SPECIAL  PA  THOLOG  Y  A  ND  TBEA  TMENT. 

is  in  the  temporal  lobe,  sensory  aphasia.  The  last-named 
symptom  may  be  absent.  Impending  rupture  (extra- 
ineningeal)  is  heralded  by  exacerbation  of  the  symptoms. 
Not  infrequently  there  are  marked  cachexia  and  apathy. 

Diagnosis. — Brain-tumor,  in  which  there  is  almost 
always  choked  disc  and  in  which  fever  is  absent,  must  be 
excluded.  The  diagnosis  rests  on  the  demonstration  of  a 
primary  purulent  focus,  the  history  of  a  previous  injury, 
meningitis  (rapid  course,  hyperesthesia,  high  fever,  rigidity 
of  the  neck),  thrombosis  of  a  sinus  (pyemic  fever),  local 
edema. 

Treatment. — Exclusively  surgical ;  trephining,  punc- 
ture with  a  probe,  opening. 

(b)  Acute  Nonsuppurative  Encephalitis. — This  in- 
cludes various  processes,  the  exact  nature  of  which  is  not 
known. 

a.  A  hemorrhagic  form,  characterized  by  the  appearance 
of  acute  inflammatory  phenomena  and  the  formation  of 
great  numbers  of  minute  inflammatory  hemorrhagic  foci  in 
the  cortex  and  basal  ganglia  (infectious  ?  toxic  ?). 

The  symptoms  are  both  meningitic  and  focal,  the  latter 
varying  according  to  the  seat  of  the  affection. 

The  prognosis  is  not  always  unfavorable. 

/?.  A  similar  form,  which  is  observed  chiefly  in  chronic 
alcoholism,  is  characterized  by  numerous  small  hemor- 
rhages in  the  brain-stem,  especially  in  the  region  of  the 
aqueduct,  underneath  the  corpora  quadrigemina.  It 
leads  to  palsies  of  the  ocular  muscles  (acute  ophthalmo- 
plegia). 

y.  An  obscure  process  that  forms  the  basis  of  so-called 
cerebral  paralysis  of  children.  This  form  of  infantile 
paralysis  is  either  congenital  or  acquired  in  earliest  infancy 
(various  processes  ?).  ^ 

Course. — During  the  first   months  of  life  the  infant  is 

^  Other  forms  of  cerebral  infantile  palsy  are  due  to  injuries  to  the 
skull  during  forceps  deliveries,  intra-uterine  circulatory  disturbances 
(endarteritis,  phlebitis),  and  various  forms  of  arrested  development. 


BRAIN-TUMOR.  149 

suddenly  seized  with  severe  meningitic  symptoms,  which, 
however,  soon  disappear.  They  depend  on  certain  inflam- 
matory processes  in  the  central  convolutions  which  have 
run  their  course  and  been  followed  by  a  formation  of  scars, 
cysts,  atrophied  areas,  and  defects  (porencephalia)  in  the 
affected  parts  of  the  brain.  Accordingly,  certain  cerebral 
palsies,  always  spastic  in  character,  remain  after  the  initial 
symptoms  have  disappeared.  If  the  lesion  is  bilateral, 
there  will  be  spastic  paraplegia.  The  growth  in  the  para- 
lyzed portion  of  the  body  (an  arm  or  a  leg,  or  one  side)  is 
much  retarded  compared  with  that  of  the  other  side,  and 
one  entire  half  of  the  body  may  remain  atrophic  (hemi- 
atrophia  spastica).  The  irritation  of  the  scar  in  the  cortex 
frequently  leads  to  epileptic  seizures  and  athetosis,  while 
psychic  defects — idiocy,  deaf-mutism,  and  defects  in  the 
speech — are  often  present. 

The  treatment  is  symptomatic.     (See  Meningitis.) 

3.  Brain^tumor. 

Tumors  may  develop  in  the  interior  of  the  brain  after 
traumatism,  as  metastatic  growths  derived  from  other 
tumors  in  the  body,  or  they  may  develop  spontaneously. 

They  may  grow  : 

Frmn  the  bone  (sarcoma,  carcinoma,  osteoma,  gumma). 

Froni  the  meninges  (sarcoma,  carcinoma,  fibroma,  soli- 
tary tubercle,  gumma). 

From  the  blood-vesseh  (gumma,  aneurysm). 

In  the  brain  substance  (glioma,  sarcoma,  metastatic  and 
primary  carcinoma,  cysticerci,  echinococci). 

The  most  frequent  tumors  in  the  adult  are  the  glioma, 
gumma,  and  sarcoma  ;  in  the  child,  the  solitary  tubercle. 

The  symptoms  vary  according  to  the  size,  the  rate  of 
growth,  the  number,  and  the  seat  of  the  tumors.  All 
tumors  have  certain  symptoms  in  common,  depending  on 
the  presence  of  a  growing  foreign  body  within  the  limited 
space  of  the  cranial  cavity.  They  are  known  as  general 
tumor  symptoms.     The  other  symptoms  depend  chiefly  on 


150  SPECIAL  PATHOLOGY  AND  TREATMENT. 

the  seat,  and  to  some  extent  on  the  variety,  of  the  tumor 
present. 

Course. — The  general  symptoms  of  brain-tumor  are 
caused  by  their  encroachment  on  the  cranial  cavity,  and 
the  resulting  increase  in  the  intracranial  pressure,  which 
exerts  an  injurious  influen(;e  both  on  the  brain  as  a  whole 
and  on  the  vascular  and  lymphatic  circulation.  These 
symptoms  are  :  (a)  Headache,  persistent,  diffuse,  dull,  and 
of  progressive  intensity,  throbbing  in  character  (/^Schet- 
tern  ");  (6)  cerebral  vomiting,  not  depending  on  the  inges- 
tion of  food  and  occurring  paroxysmally ;  (c)  vertigo, 
feeling  of  oppression,  somnolence ;  (d )  slowing  of  the 
pulse ;  (e)  ei)ileptiform  and  apoplectiform  seizures ;  (/) 
choked  dise,  or  optic  neuritis,  the  cardinal  svmptom  of  brain- 
tumor.     (See  Part  IV,  p.  118.) 

The /oca/  symptoms  are  divided  into  direct,  or  focal,  and 
indirect,  or  remote,  symptoms.  They  vary  according  to 
the  seat  of  the  growth,  and  consist  of  monoplegia,  hemi- 
plegia, sometimes  with  paralysis  of  the  cranial  nerves  of 
the  opposite  side,  hemianesthesia,  hemianopsia,  cerebellar 
ataxia  (corpora  quadrigemina,  cerebellum),  aphasia,  and 
basal  symptoms.  (For  a  detailed  account  see  under  Focal 
Diseases,  Part  IV,  3.)  Jacksonian  epilepsy  is  common. 
Tonic  and  later  clonic  convulsive  attacks  of  gradually 
increasing  extent  also  occur. 

The  focal  symptoms  may,  however,  be  absent  or,  at 
least,  very  indistinct.  Tumors  of  the  corpora  quadri- 
gemina may  produce  acute  internal  hydrocephalus  by 
pressure  on  the  veins  of  Galen  in  the  third  ventricle,  thus 
obstructing  the  flow  of  the  cerebrospinal  fluid.  (See 
Hydrocephalus,  p.  151.) 

Diagnosis. — First  of  all,  the  presence  of  a  brain-tumor 
is  diagnosticated  from  the  general  symptoms. 

The  following  conditions  are  to  be  excluded  :  Abscess 
and  hydrocephalus,  q.  r.  Next,  the  seat  of  the  tumor  is 
determined  by  attention  to  the  focal  symptoms,  as  explained 
in  Part  IV,  3,  whether  at  the  base  of  the  skull  (anterior 


HYDROCEPHALUS.  151 

middle  or  posterior  fossa),  in  one  of  the  lobes  of  the 
cerebral  hemispheres,  in  the  brain-stem  (corpora  quadri- 
gemina  or  pons),  or  in  the  cerebellum.  Only  the  direct 
focal  symptoms  which  are  persistent  and  progressive  can 
be  utilized  in  the  topical  diagnosis  ;  the  indirect  symptoms, 
or  those  that  are  transient  and  of  varying  intensity,  are 
useless  for  this  purpose.  It  is,  however,  not  always  pos- 
sible to  distinguish  between  the  two  kinds  of  symptoms. 
Finally,  an  attempt  should  be  made  to  determine  the 
nature  of  tlie  tumor  by  looking  for  signs  of  tuberculosis 
or  lues,  or  for  the  presence  of  a  primary  tumor  in  other 
parts  of  the  body.  Many  kinds  of  tumors  have  charac- 
teristic seats ;  thus,  a  tumor  at  the  base  of  the  brain  is 
either  a  gumma  or  a  sarcoma ;  gliomata  are  found  in  the 
brain  substance.  Cerebellar  and  pontine  tumors  are  usu- 
ally solitary  tubercles  or  gliomata.  The  growth  of  a  sar- 
coma is  rapid  ;  that  of  a  glioma,  slow. 

Treatment. — If  there  is  the  faintest  suspicion  of  lues, 
inunctions  and  potassium  iodid.  If  the  tumor  is  in  the  cor- 
tex, an  attempt  at  operative  removal  is  justifiable  (see 
General  Treatment) ;  otherwise  the  treatment  is  merely 
symptomatic — narcotics,  bromids. 

4.  internal  Hydrocephalus. 

By  this  term  is  meant  a  pathologic  increase  in  the 
amount  of  cerebrospinal  fluid  in  the  lateral  and  third  ven- 
tricles. The  term  external  hydrocephalus  is  applied  to  a 
collection  of  fluid  in  the  subarachnoid  space,  which  com- 
municates with  the  ventricles.  Internal  hydrocephalus 
may  be  congenital  or  acquired.  The  cause  is  supposed  to 
be  either  an  inflammatory  disease  of  the  ependyma  of  the 
ventricles  and  of  the  choroid  plexus,  or  an  obstruction  to 
the  outflow  from  the  third  ventricle  by  some  inflammatory 
change. 

In  marked  grades  of  hydrocephalus  the  cerebral  convo- 
lutions are  flattened  and  the  brain  substance  is  much 
diminished  in  quantity  and  atrophied  on  account  of  the 


152     SPECIA L  PA THOLOG Y  AND  TREA  TMENT. 

pressure.  The  circumference  of  the  skull  may  reach 
fifty  to  sixty  centimeters,  the  normal  being  less  than  fifty 
in  children.  The  collection  of  fluid  in  the  third  ven- 
tricle produces  a  bulging  of  the  floor  and  pressure  on  the 
structures  lying  beneath  it  :  optic  nerve,  chiasm  (bitem- 
poral hemianopsia),  oculomotor,  and  abducens  nerves. 

Course. — Hydrocephalus,  when  congenital  or  acquired 
in  early  childhood,  is  associated  with  idiocy,  bilateral  spas- 
tic palsies,  and  epileptiform  attacks.  Early  death  is  the 
rule.  In  adults  the  development  of  hydrocephalus  is 
accompanied  by  meningitic  phenomena  :  headache,  vomit- 
ing, coma,  optic  neuritis — but  no  fever.  The  course  is 
marked  by  exacerbations  and  remissions  ;  choked  disc  may 
be  present. 

The  diagnosis  from  brain-tumor  can  not  always  be 
made  with  certainty  (absence  of  the  increase  in  the  circum- 
ference of  the  skull,  more  rapid  development,  and  remis- 
sions not  so  frequent). 

Treatment. — Operative  :  pimcture  of  the  ventricle  or 
of  the  central  canal  at  the  lumbar  enlargement  between  the 
third  and  fourth  lumbar  vertebrae.  The  needle  should  be 
inserted  to  a  depth  of  from  seven  to  eight  centimeters  in 
an  adult.  Manometric  pressure  in  the  lateral  decubitus  is 
normally  from  forty  to  sixty  millimeters  of  water ;  a  rise 
above  150  mm.  is  pathologic.  The  value  of  these  surgical 
measures  is,  however,  very  doubtful.  Externally,  blue 
ointment ;  unguent,  tartari  stibiatis,  applied  after  shaving 
the  occiput.     Calomel. 

5.  Paralytic  Dementia  (Progressive  Paralysis). 

Progressive  paralysis  is  due  to  a  degenerative  process 
in  the  brain.  Numerous  minute,  medullated  and  non- 
medullated  nerve-fibers  and  possibly  some  cells  are  prima- 
rily destroyed,  especially  in  tlie  cortex.  The  alterations 
are  said  to  be  most  marked  in  the  frontal  lobe.  Owing  to 
the  destruction  of  the  nerve-fibers  the  thickness  of  the 
cortex  gradually  diminishes,    and  ultimately  the   entire 


PA  RA  L  YTIC  DEMENTIA .  153 

brain  becomes  atrophied.  In  addition  to  this  degenerative 
process  chronic  inflammatory  changes  in  the  vessels,  the 
neuroglia,  and  the  meninges,  and  internal  hydrocephalus, 
etc.,  are  constantly  present. 

The  disease  is  particularly  common  in  men.  It  shows 
a  remarkable  tendency  to  follow  syphilis,  and  shares  with 
tabes  the  appellation  mdasyphilw.  It  is  also  known  to 
follow  traumatism. 

Course. — The  degeneration  of  the  nervous  elements  in 
the  cortex  is  attended  with  progressive  deterioration  of  the 
mental  functions,  the  intelligence,  the  character,  the  mem- 
ory, and  the  power  of  speech  (associative  functions). 

Symptoms. — The  change  in  the  character  is  often  the 
first  prominent  symptom  :  Dullness,  irritability,  tendency 
to  commit  excesses,  inability  to  do  any  mental  work,  de- 
pravity. If  the  patient  presents  himself  during  this 
period,  the  following  characteristic  symptoms  are  to  be 
specially  looked  for. 

1.  Rigidity  of  the  pupik^  either  unilateral  or  bilateral ; 
unequal  pupils. 

^.  Paralytic  distarhances  of  speech  (literal  paraphasia)  : 
negligent,  incorrect  manner  of  speaking,  omission  or  trans- 
position of  letters  and  syllables.  (See  under  Disturbances 
of  Speech,  Part  IV,  4.)  Or  agraphia  and  alexia  may  be 
present — letters,  syllables,  or  words  may  be  omitted  or 
punctuation  marks  put  in  the  wrong  places. 

3.  Loss  of  Patellar  Reflex. — Paralytic  dementia  may 
occur  in  connection  with  tabetic  symptoms ;  or  it  may  be 
associated  with  disease  of  the  lateral  tracts,  in  which  case 
the  reflexes  will  be  exaggerated. 

^.  Tremor  of  the  hands,  and  of  the  tongue  and  lips  while 
speaking. 

The  paralytic  attacks  occur  later  in  the  disease.  There 
may  be  apoplectiform  disturbances  of  consciousness,  with 
or  without  epileptiform  seizures.  The  concomitant  paral- 
ytic symptoms  usually  disappear  as  the  attack  passes  off. 

The  psychic  deteriomtion  goes  steadily  on,  and  finally 


154  SPECIA  L  PA  THOLOG  Y  AND  TEE  A  T3IENT. 

leads  to  delusions  of  grandeur  and  attacks  of  mania.  The 
disease  is  marked  by  long  periods  of  remission,  during 
which  the  patient  appears  to  regain  his  normal  condition, 
but  the  malady  soon  breaks  out  again  with  renewed  inten- 
sity. In  the  final  stages  the  subject  becomes  totally  de- 
mented and  sinks  into  a  brutish  state.  Death  occurs  from 
exhaustion  or  inspiration  pneumonia  after  a  period  varying 
from  a  few  months  to  two  or  three  years. 

Diagnosis. — Paralytic  dementia  must  be  differentiated 
from  severe  neurasthenia  (persistent  absence  of  the  objec- 
tive symptoms)  ;  multiple  sclerosis,  q.  v. ;  brain  syphilis 
(pronounced  focal  symptoms). 

The  treatment  is  best  carried  out  in  an  institution ;  it 
is  purely  symptomatic.  Antisyphilitic  treatment  is  rather 
harmful  than  beneficial. 

6.  Ophthalmoplegia. 

Bilateral  paralysis  of  the  ocular  muscles  from  disease 
situated  in  the  nuclei  of  the  oculomotor  nerve,  beneath  the 
corpora  quadrigemina,  occurs  in  a  variety  of  diseases. 

(a)  Acute  Ophthalmoplegia. — Among  the  causes  other 
than  the  above-mentioned  hemorrhagic  encephalitis  are 
other  hemorrhagic  embolic  processes  following  heart 
disease,  syphilis,  alcoholism,  arteriosclerosis,  etc.,  and 
tumors. 

(b)  Chronic  Progressive  Ophthalmoplegia. — Like 
bulbar  paralysis,  which  will  be  discussed  in  the  following 
section,  this  belongs  to  the  system  diseases  of  neuron 
cells.  (See  Part  IV,  3.)  There  is  a  slowly  progressive 
atrophy  in  the  cells  of  the  oculomotor  nucleus,  which  in 
the  course  of  years  leads  to  total  paralysis  of  all  the  exter- 
nal, and  rarely  of  the  internal,  muscles  of  the  eyeball. 
The  oculomotor  fibers,  of  course,  disappear  also. 

The  disease  occurs  either  by  itself  or  as  a  concomitant 
of  tabes,  paralytic  dementia,  bulbar  palsy,  and  multiple 
sclerosis. 

Treatment. — Antisyphilitic,  if  indicated. 


BULBAR  PARALYSIS.  155 

7.  Bulbar  Paralysis. 

(a)  The  acute  form  may  be  due  to  thrombosis,  em- 
bolism, or  to  inflammatory  or  hemorrhagic  processes. 

Symptoms. — The  onset  of  the  symptoms  is  usually 
sudden,  as  in  apoplexy.  They  consist  in  paralysis  of  the 
muscles  of  the  tongue  and  pharynx,  disturbances  of  pho- 
nation  and  respiration,  and  paralysis  of  the  facial,  abducens, 
and  trifacial  nerves.  Bulbar  speech,  paralysis  of  the 
extremities,  and  sudden  death  from  failure  of  heart  and 
respiration. 

(b)  Chronic  Progressive  Bulbar  Paralysis. — Morbid 
Anatomy. — The  anatomic  basis  is  a  slowly  progressive 
destruction  of  the  cells  of  the  nuclei  situated  in  the  medulla 
oblongata,  especially  in  the  motor  nuclei  (peripheral  neuron 
cells)  of  the  hypoglossus,  facial,  vagus,  spinal  accessory, 
and  trifacial  nerves.  The  pyramidal  tract  and  the  ante- 
rior horns  of  the  spinal  cord  are  frequently  involved, 
hence  any  intermediate  form  between  simple  bulbar  paral- 
ysis and  amyotrophic  sclerosis  with  bulbar  symptoms  may 
occur.     (See  under  System  Diseases.) 

Concerning  the  etiology,  very  little  is  known. 

Gourse. — The  clinical  phenomena  develop  very  gradu- 
ally. First  certain  bulbar  disturbances  of  the  speech  are 
noticed,  the  letters  r,  s,  and  /  being  less  distinctly  pro- 
nounced. Later,  there  develop  a  bilateral  atrophy  (RD) 
and  paresis  of  the  lips,  tongue  (fibrillary  contractions),  the 
muscles  concerned  in  deglutition  and  phonation,  and, 
rarely,  of  the  muscles  of  mastication.  Finally,  complete 
rigidity  of  the  muscles  of  expression  (the  lower  facial  only 
is,  as  a  rule,  involved),  salivation,  and  inability  to  swallow 
or  articulate  (anarthria)  occur.  There  are  no  sensory 
disturbances. 

There  may  be  psychic  alterations,  such  as  constant  ten- 
dency to  weep,  etc.  ;  and  if  other  systems,  as  the  pyra- 
mids, are  involved,  spastic  paralysis  of  the  extremities  and 
atrophy  of  the  muscles  of  the  hand  may  occur.    (See  Amyo- 


156  SPECIAL  PATHOLOGY  AND  TREATMENT. 

trophic  Lateral  Sclerosis.)    The  patients  die  of  asthenia  or 
inspiration  pneumonia. 

Treatment. — Symptomatic  ;  electricity,  baths,  tubal 
feeding.  Arsenic,  strychnin,  potassium  iodid,  and  atropin 
are  without  effect.  It  is  impossible  either  to  replace  the 
ganglion  cells  that  have  been  destroyed  or  to  arrest  the 
progress  of  the  disease. 

Bulbar  paralysis  may  be  simulated  by  other  diseases. 

(a)  Pseudobulbar  paralysis  is  due  to  softening  foci  from  embolus 
or  hemorrhage  in  corresponding  regions  of  the  two  cerebral  hemi- 
spheres. If  the  centers  for  the  facial,  hypoglossus,  etc.,  are  injured, 
the  symptoms  of  bulbar  paralysis  without  muscular  atrophy  may  be 
produced.  It  is  to  be  remembered,  however,  that  other  diseased  foci 
may  be  present  in  the  medulla  at  the  same  time. 

(b)  Bulbar  Paralysis  Without  any  Pathologic  Changes.— 
The  disease  is  a  combination  of  bulbar  symptoms  with  paretic  con- 
ditions of  other  extremities,  etc.  The  muscles  readily  become  fatigued ; 
paresis  may  be  present,  but  without  atrophy.  Up  to  the  present  time 
no  anatomic  basis  has  been  discovered  for  the  disease. 

It  is  not  always  possible  to  exclude  these  forms,  espe- 
cially in  the  diagnosis  of  an  acute  disease.  Hysteria  and 
multiple  sclerosis  under  certain  conditions  may  produce  a 
similar  clinical  picture.  The  above-mentioned  points  in 
the  diagnosis  should,  therefore,  receive  the  most  careful 
attention.  The  most  characteristic  feature  of  the  symptom- 
complex  is  its  gradually  progressive  development. 

8.  Diseases  of  the  Cerebellum. 

These  have  been  discussed  under  Tumor  and  Abscess. 
Other  diseases  of  the  cerebellum,  such  as  atrophy  and 
sclerosis,  are  rare. 

9.  Multiple  Cerebrospinal  Sclerosis. 

See  under  Diseases  of  the  Spinal  Cord. 


CEREBRAL  NEUROSES.  157 


B.  CEREBRAL   DISEASES  OF  UNKNOWN   CHARACTER 
AND   LOCALIZATION. 

Cerebral  Neuroses. 

This  term  embraces  all  those  diseases  of  the  brain  the 
exact  nature  and  seat  of  which  are  unknown. 

I.  Neurasthenia. — Neurasthenia,  with  hysteria  and 
hypochondria,  represents  the  transition  to  grave  psychic 
diseases  (psychoses).  Neurasthenia  is  a  chronic  condition 
of  morbid  asthenia  and  irritability  of  various  psychic  and 
bodily  functions,  due  to  improper  training  and  bringing-up, 
to  overexertion  and  excesses  of  all  kinds,  and  is,  in  many 
cases,  dependent  on  hereditary  predisposition. 

Symptoms. — The  patient  is  depressed  or  anxious  and 
irritable ;  the  will  power  and  the  capacity  for  work  are 
impaired,  particularly  such  work  as  requires  mental  con- 
centration. Among  other  symptoms  may  be  mentioned  : 
fatigue  after  the  slightest  exertion  ;  a  morbid  tendency 
to  introspection  (nosophobia,  syphilophobia) ;  insomnia  ; 
feeling  of  oppression  in  the  head  ;  tremors  and  palpita- 
tion. 

The  clinical  picture  may  be  in  addition  complicated  by 
a  long  array  of  other  physical  symptoms  ;  abnormal  sensa- 
tions of  every  kind  ;  pains  ;  disturbances  of  the  gastric  and 
intestinal  functions  (liyperacidity,  nervous  dyspepsia)  and 
of  the  sexual  power.  (Consult,  in  this  connection,  the 
paragraph  on  Occupation  Neuroses,  p.  189.) 

In  severe  grades  of  neurasthenia  the  patient  is  harassed 
by  uncontrollable  thoughts  and  metaphysical  mania,  but  the 
condition  does  not  develop  into  any  other  psychic  affection. 
The  typical  course  of  neurasthenia  is  intermittent :  the 
patient  may  feel  quite  well  for  a  long  time,  when  suddenly 
the  distressing  symptoms  again  make  their  appearance  in 
full  force. 

Diagnosis. — Exclude  other  bodily  diseases,  such  as 
paralytic  dementia,  multiple  sclerosis,  and  hysteria,  by 
repeated  careful  examination  (urine,  lungs,  heart,  stomach). 


158  SPECIAL  PATHOLOGY  AND  TREATMENT. 

The  differential  diagnosis  from  these  three  diseases  will  be 
found  under  the  respective  headings. 

Treatment. — Allay  the  patient's  fears  and  forebodings 
as  much  as  possible  and  give  him  moral  encouragement. 
A  neurasthenic  patient  should  always  be  carefully  ex- 
amined ;  it  is  a  great  mistake,  both  from  a  therapeutic  and 
diagnostic  point  of  view,  to  send  him  away  without  a 
minute  objective  examination,  for  such  a  patient  is  really 
ill.  Give  abundant  and  nutritious  diet ;  cold  baths  or 
change  of  air,  either  at  the  seashore  or  at  the  mountains  ; 
Weir  Mitchell's  treatment  (four  weeks  in  bed  on  a  diet  of 
milk,  eggs,  and  large  quantities  of  meat) ;  electricity ; 
gymnastic  exercise ;  arsenic,  iron,  quinin.  Do  not  give 
too  much  medicine — no  morphin. 

2.  Hypochondria. — This  aifection  shares  with  neuras- 
thenia the  symptom  of  morbid  introspection ;  but  whereas 
in  neurasthenia  the  patient's  complaints  as  to  the  location 
and  intensity  of  the  pain  vary  from  time  to  time,  the  sen- 
sations complained  of  in  hypochondria  are  more  constant 
and  localized.  As  a  rule,  the  patient  complains  of  some 
disturbances  of  the  abdominal  functions.  The  effect  of 
these  sensations  on  the  psychic  condition  is  more  lasting 
and  more  systematized  ;  in  fact  the  depression  of  hy[)o- 
chondria  is  much  deeper  seated  than  that  of  neurasthenia. 
A  neurasthenic  discusses  his  symptoms  with  the  greatest 
frankness,  while  the  hypochondriac  broods  over  his  troubles 
in  sullen  taciturnity. 

Gastro-intestinal  disease  (latent  carcinoma,  tapeworm) 
is  to  be  excluded.  Hypochondria  can  be  distinguished 
from  beginning  paranoia  and  the  systemic  delusions  char- 
acteristic of  that  condition  only  by  careful  observance  of 
the  progress  of  the  disease. 

The  treatment  is  the  same  as  for  neurasthenia. 

3.  Hysteria. —  Definition. —  Hysteria  is  a  psychosis 
due  to  some  morbid  disturbance  of  volition  and  psychic 
representation,  manifesting  itself  in  an  endless  variety  of 
functional  anomalies  of  the  motor  and  sensory  spheres,  for 


HYSTERIA.  1 59 

which  it  is  impossible  to  discover  any  organic  basis.  The 
manifestations  of  tlie  disease  are  all  purely  psychogenic  in 
origin. 

Course. — Hysteria  occurs  most  frequently  in  young 
individuals.  The  most  important  factors  in  the  etiology 
are  heredity,  education,  and  emotional  disturbances. 

The  psychic  condition  in  hysteria  undergoes  a  morbid 
change,  so  that  the  patients,  either  by  suggestion  or  auto- 
suggestion, exhibit  a  variety  of  psychic  and  bodily  reac- 
tions. They  are  irritable,  capricious,  absent-minded,  and 
very  uncertain  in  their  actions  (explosive  actions)  ;  the 
intelligence  is  not  affected. 

The  bodily  symptoms  are  (1)  stigmata,  which  are  perma- 
nent, but  may  be  absent,  and  (2)  paroxysmal  hysteric 
attacks. 

1.  Stigmata. — (a)  Hemianesthesia,  or  total  loss  of  sensa- 
tion of  one  half  the  body  or  of  individual  regions,  includ- 
ing all  the  qualities  of  sensation,  pain,  heat,  etc.  The  sense 
of  taste,  smell,  and  hearing  may  be  lost  on  the  same  side 
and  the  color-sense  may  be  impaired  (achromatopsia). 
The  visual  field  may  be  contracted  or  there  may  be  an 
unusual  tendency  to  ocular  fatigue.  The  hemianesthesia 
is  due  to  loss  of  a  part  of  the  associations  necessary  for 
conscious  sensation. 

(b)  Hyperesthesia  of  one  half,  or  part  of  one  half,  of 
the  body,  pain  elicited  by  pressure  on  the  ovaries,  the 
groin,  the  patella,  and  vertebral  pain.^  Hysteric  attacks 
can  be  produced  by  irritation  of  these  points  (hysterogenic 
zones — loss  of  central  associative  inhibition). 

Pains  and  abnormal  sensations  of  various  kinds,  such 
as  globus  hystericus,  etc.,  are  often  complained  of. 

(c)  Hysteric  palsies,  which  may  simulate  almost  any 
form  of  disease.  They  are  due  to  a  central  paralysis  of 
the  will  power  (paralysis  of  certain  movements,  not  of 

^  This  tenderness  on  pressure,  however,  is  often  present  in  healthy 
individuals  and  may  also  be  suggested  by  the  physician's  repeated  ex- 
aminations. 


1 60  SPECIA  L  PA  THOLOG  Y  A  ND  TREA  TMENT. 

individual  muscles),  and  may  disappear  as  rapidly  as  they 
came. 

The  most  common  forms  are  hysteric  aphonia,  agraphia, 
aphasia,  aphagia,  hysteric  hemiplegia  (without  involve- 
ment of  the  facial  and  hypoglossus),  hysteric  astasia  (in- 
ability to  stand),  and  abasia  (inability  to  walk) ;  forced 
movements  of  various  kinds  ;  retention  of  urine. 

(d)  Hysteric  Contractures. — These  are  due  to  central 
irritation  of  a  purely  functional  character.  The  greatest 
variety  of  contractures,  either  of  the  flexors  or  of  the 
extensors,  is  observed,  involving  either  the  head  or  the 
extremities. 

2.  Hysteric  Attacks. — Central  irritative  phenomena, 
manifesting  themselves  in  a  great  variety  of  different  forms 
and  combinations  and  occurring  either  spontaneously  or  as 
the  result  of  a  kind  of  reflex  excitation  (fright,  emotion, 
sensation,  etc.).  Clonic  and  tonic  convulsions  of  the  ex- 
tremities and  of  the  trunk  follow  each  other  in  rapid 
succession.  There  is  gasping  respiration  or  dyspnea ; 
consciousness  is  rarely  affected  to  any  marked  degree, 
although  the  patient  does  not  remember  anything  about 
the  attacks  (amnesia).  During  the  convulsions  the  patient 
may  assume  a  number  of  grotesque  attitudes  in  rapid 
succession  (clownism,  ''arc  de  cerck^-),  while  the  limbs 
execute  the  most  peculiar  movements  (grand  hysteria). 
Trismus,  choking  fits,  and  hysteric  attacks  of  laughing 
and  weeping  may  be  more  or  less  pronounced.  During 
the  attacks  the  patient  often  has  pleasant  or  unpleasant 
hallucinations,  which  impel  her  to  shout  or  call  names  or 
to  gesticulate  wildly  and  make  faces. 

Coma,  such  as  is  observed  in  epileptic  attacks,  never 
occurs ;  the  reflexes  are  preserved.  In  ordinary  attacks 
the  patient  can  be  roused  by  sprinkling  the  face  with 
water,  and  even  if  the  attack  is  severe,  a  painful  prick 
in  the  sole  of  the  foot  with  a  needle  will  almost  always 
suflice  to  rouse  her. 

Characteristic  features  of  hysteric  attacks  are  the  exag- 


HYSTERIA.  161 

gerated  eifect  and  changeable  nature  of  the  convulsions 
and  the  fact  that  the  attacks  can  be  induced  and  prevented 
by  appropriately  influencing  the  patient  by  suggestion. 

A  number  of  diseases,  some  of  which  are  known  by 
separate  names,  are  included  in  the  category  of  psychogenic 
conditions:  Akinesia  algera,  or  pain  on  motion,  without 
any  recognizable  cause,  and  hence  inability  to  move  a  part ; 
chorea  electrica,  or  forced  spasmodic  movements  of  the 
body  ;  paramyoclonus  multiplex,  clonic  muscular  contrac- 
tions occurring  alternately  in  various  parts  of  the  body 
(biceps,  quadriceps,  supinator  longus,  trapezius,  etc.) ; 
astasia  and  abasia  (g.  i\). 

The  diagnosis  can  be  arrived  at  only  by  keeping  the 
entire  clinical  picture  of  hysteria  in  mind — a  single  sym}> 
tom  does  not  suffice  ;  by  a  careful  examination  the  presence 
of  stigmata  and  the  occurrence  of  attacks  can  usually  be 
discovered.  It  is  not  always  possible  to  distinguish  hys- 
teria from  neurasthenia,  but  in  most  cases  some  one  symp- 
tom will  decide  between  the  two  conditions.  In  severer 
forms  psychic  disturbances  may  be  more  pronounced  (moral 
defects). 

Treatment. — The  treatment  for  the  most  part  must  be 
psychic ;  the  patient  should  be  encouraged  to  follow  some 
regular  occupation.  An  attempt  should  be  made  to  re- 
store her  confidence  in  her  own  will  power  ;  if  possible, 
she  should  be  removed  to  an  institution,  where  she  will 
be  away  from  nervous  and  overanxious  members  of  her 
family.  The  attacks  should  be  made  light  of;  the  diet, 
of  course,  should  be  regulated,  and  baths  and  douches 
should  be  ordered.  In  some  cases  iron  and  bromid  are 
indicated,  but  their  usefulness  bears  no  proportion  to  that 
of  the  moral  treatment.     Morphin  should  never  be  given. 

Hypnotic  treatment,  as  a  rule,  only  removes  individual 
symptoms  and  rarely  brings  about  complete  cure  of  the 
malady.  In  many  cases  it  is  the  means  of  bringing  new 
symptoms  into  existence.  It  is  much  better  to  depend  on 
a  rational  and  not  directly  hypnotic,  but  merely  psychic, 
11 


162  SPECIAL   PATHOLOGY  AND    TREATMENT. 

suggestion.  (Slight  deceptioDs  are  permissible  and,  indeed, 
very  useful — so-called  suggestions  during  the  waking 
state.) 

4.  Traumatic  Neuroses. — The  cases  belong  in  part  to 
neurasthenia,  in  part  to  hypochondria  and  hysteria.  They 
have  this  in  common  that  they  are  produced  by  some 
psychic  or  physical  injury,  usually  in  patients  predisposed 
by  heredity  or  alcoholism. 

In  view  of  the  possibility  of  exploiting  the  disease  as  a 
means  of  revenue  from  accident-insurance  policies,  patients 
of  this  kind  are  very  difficult  to  treat.  It  is  often  ex- 
ceedingly difficult  to  draw  the  line  between  intentional 
exaggeration  and  morbid  psychic  inhibition.  For  thera- 
peutic reasons  it  is  well  to  be  guarded  at  first  in  determin- 
ing the  degree  of  disability.  A  definite  opinion  should  be 
given  only  in  exceptional  cases ;  as  a  rule,  it  should  be 
withheld  until  the  patient  has  been  examined  repeatedly. 
In  this  class  belong  the  neuroses  after  railway  accidents — 
railway  spines  and  other  conditions. 

For  the  treatment  see  under  Neurasthenia  and  Hys- 
teria. 

5.  Hemicrania  and  Migraine. — This  consists  in  peri- 
odic attacks  of  violent  headache,  confined  to  one  side  of  the 
head  and  associated  with  nausea  and  vomiting.  It  may 
occur  by  itself,  but  is  more  frequently  associated  with  other 
nervous  symptoms  and  is  often  dependent  on  hereditary 
predisposition.  The  attacks  may  be  produced  by  reflex 
irritation  (diseases  of  the  nose,  stomach,  or  genitalia). 
The  frequency  and  duration  of  the  attacks  are  subject  to 
wide  variations.  The  attack  may  be  preceded  or  accom- 
panied by  visual  disturbances,  such  as  flashes,  scotomata, 
diminution  in  the  visual  field.  Hyperacidity  is  often 
present  (toxic  eflect?). 

Treatment. — Carlsbad  or  other  baths,  iron,  arsenic,  and 
removal  of  the  exciting  cause.  Symptomatic.  Antinervin, 
citrophen,  antipyrin,  cafPein,  or  combinations  of  these  ;  mus- 
tard foot-baths  ;  compresses  ;  rest.     Never  give  morphin. 


EPILEPSY.  163 

6.  Cephalalgia  (Habitual  Headache). — Headache  is 
frequently  only  a  concomitant  symptom  of  otlier  disease 
(fever,  circulatory  disturbance,  intoxications,  tumors)  ;  it 
may,  however,  in  nervous  individuals  constitute  the  most 
prominent  symptom. 

In  the  diagnosis  we  must  exclude,  in  addition  to  the 
above-named  conditions,  disease  of  the  nasal  and  frontal 
cavities  and  diseases  of  the  eyes  (myopia,  astherlopia,  etc.). 

For  the  treatment,  antinervin  ;    see  also  Neurasthenia. 

7.  True  Epilepsy. — By  the  term  epilepsy  is  meant 
the  periodic  appearance  of  the  so-called  epileptic  convul- 
sions. True  epilepsy  is  to  be  distinguished  from  the 
symptomatic  form,  or  Jacksonian  epilepsy,  which  has  been 
referred  to  repeatedly  in  the  section  on  Focal  Diseases  of 
the  Brain. 

The  epileptic  attacks  are  thought  to  originate  in  the  cor- 
tex, particularly  in  the  central  convolutions  ;  their  cortical 
origin  is,  however,  not  generally  admitted.  The  attacks 
are  originally  excited  by  the  irritation  of  an  injured  spot 
in  the  cortex  (scar,  spicule  of  bone,  inflammatory  process)  ; 
this  is  at  least  very  probable  in  the  symptomatic  form, 
and  is  supposed  to  be  the  case  also  in  true  epilepsy.  From 
the  original  focus  the  irritation  is  transmitted,  through  the 
association  tracts,  to  neighboring  centers,  and  thus  pro- 
duces the  epileptic  convulsion. 

The  etiologic  factors  in  the  production  of  true  epilepsy 
are  heredity,  traumatism,  and  infectious  diseases.  The 
disease  often  appears  in  childhood,  and  may  vary  greatly 
in  respect  to  duration  and  intensity.  The  epileptic  attacks 
may  be  severe  or  mild  in  character  {grand  mal — petit  mal) 
or  the  attack  may  take  the  form  of  a  stuporous  condition. 

Attack. — A  typical  attack  begins  with  an  aura  (head- 
ache, nausea,  vertigo,  visual  and  auditory  sensations), 
which  is  immediately  followed  by  the  seizure.  The  patient 
falls  to  the  ground  unconscious,  and  is  thrown  into  a  tonic 
convulsion  aflecting  chiefly  the  extensor  and,  to  some 
extent,  the  flexor  muscles  of  the  entire  body.     All  the  re- 


164  SPECIAL  PATHOLOGY  AND  TREATMENT. 

flexes  are  abolished,  and  the  pupils  are  dilated.  After  a 
time  (about  half  a  minute)  this  condition  is  succeeded  by 
the  clonic  stage,  characterized  by  violent  forced  contrac- 
tions of  the  extremities  and  muscles  in  other  parts  of  the 
body.  The  patient  bites  his  tongue  and  foams  at  the  mouth. 

After  a  few  minutes  the  force  of  the  convulsion  spends 
itself,  and  the  patient  falls  into  a  comatose  condition,  from 
which  he  awakes  after  a  variable  interval  of  time.  Head- 
ache, nausea,  and  fatigue  may  persist  for  some  time  after 
the  attack.  The  patient  does  not  remember  anything  that 
occurs  during  the  attack.  In  the  milder  attacks  the 
tonic  and  clonic  stages  are  not  so  well  marked,  and  in  the 
equivalents  there  is,  instead  of  an  attack,  a  momentary 
dazed  condition  (^'  Dammerzustand ''),  which  may  be 
accompanied  by  maniacal  seizures,  delirium,  and  halluci- 
nations. The  attacks  occur  most  frequently  during  the 
night  (epilepsia  nocturna).  When  they  occur  with  great 
frequency,  the  condition  is  not  without  danger  and  is 
known  as  etat  de  mal  (status  epilepticus).  In  some,  but 
not  by  any  means  in  all,  cases  the  attacks,  if  they  persist 
for  a  number  of  years,  eventually  lead  to  a  psychic  degen- 
eration. 

In  the  diagnosis  we  must  exclude  hysteric  attacks  {q. 
v.)j  Jacksonian  epilepsy  (focal  symptoms  during  the  inter- 
vals of  attack),  uremic  attacks  (examination  of  urine), 
simulation  (reflexes  not  abolished — prick  the  patient  in  the 
sole  of  the  foot),  and  attacks  of  paralytic  dementia  (his- 
tory, attacks  are  of  longer  duration). 

Treatment. — Potassium  l)romid  (one  to  four  drams  per 
diem)  ;  opium,  IJ  to  15  grains  per  diem,  given  some  time 
before,  is  often  of  service  when  the  attacks  are  frequent. 
Cold  baths.  No  alcohol.  Vegetable  diet.  If  the  focal 
symptoms  are  very  marked,  operative  interference  may  be 
considered. 

8.  Eclampsia  Infantum. — During  the  first  years  of 
life  general  convulsions  may  make  their  appearance  in  the 
course  of  a  great  variety  of  diseases  (gastro-intestinal  dis- 


SYDENHAM'S  CHOREA.  165 

eases,  dentition,  fever,  rickets).  Their  occurrence  is  ex- 
plained by  deficiency  of  the  reflex  inhibitory  apparatus 
in  the  infantile  nervous  system. 

The  convulsions  consist  in  alternate  tonic  and  clonic 
contractions  of  the  entire  body.  The  children  often  cry 
out  convulsively.  In  rare  cases  the  condition  is  later  fol- 
lowed by  epilepsy. 

Diagnosis. — Exclude  tubercular  meningitis  (basal  symp- 
toms, fever). 

Treatment. — Correct  the  primary  condition  (worms,  im- 
proper feeding)  ;  pack  with  wet  cloths ;  cutaneous  irrita- 
tion ;  douches  ;  cold  sponging. 

9.  Chorea  Minor  (St.  Vitus*  Dance ;  Sydenham's 
Chorea). — This  is  a  disease  of  youth.  Nothing  is  known 
either  of  its  origin  or  of  its  seat  (cortex  ?  optic  thalamus  ?)  ; 
it  is  usually  thought  to  be  of  infectious  origin.  Its  fre- 
quent occurrence  in  acute  rheumatic  polyarthritis  and 
rheumatic  endocarditis  is,  to  say  the  least,  suggestive.  It 
not  infrequently  occurs  during  pregnancy,  when  it  is  likely 
to  be  unusually  violent. 

Course. — The  chorea  consists  in  involuntary,  incessant, 
and  irregular  movements  of  the  fingers,  hands,  arms,  legs, 
head,  facial  muscles,  etc.  All  the  muscles  that  are  usu- 
ally under  the  control  of  the  will  exhibit  a  constant  rest- 
lessness, so  that  it  is  impossible  for  the  child  to  maintain 
the  body  or  the  extremities  in  the  same  position  for  any 
length  of  time. 

The  symptoms  in  individual  cases  vary  from  scarcely 
perceptible  choreic  movements  of  the  fingers,  often  mis- 
taken for  wilful  misbehavior  in  the  school-room,  to  pro- 
nounced muscular  mania  (^folie  musculaire).  In  severe 
cases  of  this  kind  the  child  may  be  unable  to  speak,  walk, 
or  eat.  Chorea  is  sometimes  unilateral  (hemichorea,  also 
called  transitory  hemiparesis).  The  restlessness  disappears 
during  the  night.  The  disease  may  last  from  a  few  months 
to  several  years  ;  relapses  are  common  ;  in  the  end,  how- 
ever, almost  all  cases  recover. 


166  SPECIAL  FA  THOLOG  Y  A ND  TREA  TMENT. 

Treatment. — Arsenic,  antipyrin  (eight  to  sixteen  grains 
three  times  a  day),  salol,  massage,  diet.  The  child  should 
be  kept  out  of  school. 

10.  Chronic  Hereditary  Chorea  (Huntingdon's 
Chorea). — This  is  an  entirely  different  disease  from  chorea 
minor.  Its  true  nature  is  still  unknown.  It  occurs  later 
in  life  in  individuals  predisposed  by  heredity,  and  is  char- 
acterized by  motor  irritative  phenomena  and  isolated  con- 
tractions, which  in  the  course  of  years  increase  in  extent 
and  intensity.  Pari  passu  there  is  progressive  decay  of 
the  mental  faculties.  As  far  as  known,  recovery  has  never 
occurred. 

11.  Paralysis  Agitans  (Parkinson's  Disease). — The 
disease  usually  makes  its  appearance  in  advanced  age. 
Nothing  is  known  of  its  nature.  It  is  supposed  to  be 
caused  by  emotions  and  mental  worry. 

The  affection  begins  with  a  peculiar  slow,  rhythmic 
tremor  (five  to  six  beats  a  minute)  of  the  arm  and  hands, 
similar  to  the  motion  made  in  rolling  pills.  The  tremor 
persists  when  the  patient  is  at  rest.  It  is  aggravated  by 
excitement.  As  the  years  go  on  the  tremors  become  more 
extensive.  All  the  extremities,  the  head,  and  the  lips 
become  involved,  and  the  patient  assumes  a  characteristic 
attitude,  with  the  head  bent  forward,  the  back  bowed,  and 
the  arms  slightly  flexed  at  the  elbows.  During  sleep  the 
tremors  usually  subside.  Eventually  paralytic  symptoms 
make  their  appearance.     The  disease  is  incurable 

Treatment. — Rest,  good  food,  bromids. 

12.  Congenital  Myotonia  (Thomsen's  Disease). — 
This  is  a  rare  affection,  hereditary  in  character.  All  the 
voluntary  movements,  especially  walking,  are  impeded  by 
spastic  contractions,  occurring  spontaneously.  The  rigid- 
ity of  the  muscles  is  increased  by  mental  emotion  (resem- 
bles stammering). 

Treatment. — Baths  ;  gymnastic  exercise. 

13.  Idiopathic  Tremor. — A  tremor  is  not  infrequently 
observed  in  the  head  and  extremities  in  healthy  individuals 


HYPERTROPHIC  CERVICAL  PACHYMENINGITIS.     167 

with  perhaps  a  slight  neurasthenic  taint.     The  condition 
is  not  rarely  hereditary  and  is  aggravated  by  excitement. 
Treatment. — See  Neurasthenia.     The  extremities  may 
be  tied  fast ;  massage. 

III.   DISEASES  OF  THE  SPINAL  CORD. 

A.  DISEASES  CAUSED  BY  FOCAL  LESIONS  INVOLVING 
A  CROSS=SECTION  OF  THE  CORD. 

Diseases  of  the  Spinal  Meninges. 

Disease  of  the  spinal  meninges  is  usually  associated  with 
inflammatory  processes  in  the  cerebral  portion  of  these 
structures  ;  it  is  rarely  isolated.  The  meninges  are  in- 
volved most  frequently  in  cerebrospinal  meningitis  and  in 
purulent  meningitis ;  more  rarely  they  are  the  seat  of 
tubercular  lesions.  The  anatomic  changes  are  the  same  as 
in  the  cerebrum. 

The  clinical  symptoms  are  often  quite  overshadowed  by 
those  which  are  due  to  the  cerebral  condition.  The  fol- 
lowing symptoms  are  thought  to  be  due  to  irritation  of  the 
spinal  roots  (reflex  through  the  posterior  or  direct  from 
the  anterior  ?) :  Rigidity  of  the  nuchal  muscles  (roots  of 
the  upper  portion  of  the  cervical  enlargement),  opisthotonos 
(thoracic  portion),  hyperalgesia  (radiating  pains),  paralysis 
of  the  bladder.  The  spinal  origin  of  these  symptoms  is 
not  quite  definitely  settled.  In  many  instances  it  is  not 
possible  to  exclude  the  influence  of  cerebral  disease. 
Among  the  idiopathic  forms  we  have  : 

I.  Hypertrophic  Cervical  Pachymeningitis. — This 
consists  in  a  marked  inflammatory  thickening  of  the  dura, 
especially  in  the  region  of  the  cervical  cord,  forming  adhe- 
sions with  the  pia-arachnoid,  and  leading  to  compression 
of  the  cervical  nerve-roots  and  cord.  The  cause  is  un- 
known (syphilis  ?). 

The  symptoms  are  those  of  a  focal  disease  in  the 
cervical  enlargement  (see  Part  IV,  3),  the  symptoms  of 
irritation  of  the  nerve-roots  being  particularly  marked  : 


168 


SPECIA  L  PA  THOL  OG  Y  AND  TREA  TMENT. 


Violent  neuralgic  pains  in  the  back  of  the  neck  and  scapu- 
lar region,  paralysis,  and  muscular  atrophy,  most  pro- 
nounced in  the  muscles  supplied  by  the  ulnar  and  median 
nerves — i.  e.,  the  small  muscles  of  the  hand  and  the  flexor 
muscles.  The  contraction  of  the  antagonistic  groups  of 
radial  muscles  produces  the  so-called  iyreaGher''s  hand.  In 
rare  cases  the  gait  is  spastic  and  the  bladder  function  is 
impaired.      Improvement  is  possible. 

Treatment. — Antisyphilitic.  Electricity.  Symptomatic. 
Cauterization  of  the  back  of  the  neck. 

2.  Syphilitic  Spinal  Meningomyelitis. — The  soft 
membranes  of  the  spinal  cord  become  the  seat  of  super- 
ficial gummatous  neoplasms, 
seen  with  the  naked  eye  as 
a  thick,  jelly-like  deposit, 
similar  in  appearance  to 
those  seen  in  brain  syphilis, 
with  which  the  disease  may 
or  may  not  be  associated. 
These  deposits  may  com- 
press the  spinal  cord  by  sur- 
rounding it  in  its  entire 
circumference,  as  seen  in 
Figure  27,  or  they  may 
extend  into  the  cord  sub- 
stance. The  disease  attacks  most  frequently  the  thor- 
acic portion  of  the  cord.  The  arteries  exhibit  tlie  same 
changes  as  in  syphilitic  endarteritis  in  the  cerebrum.  The 
neoplasm  extends  into  the  nerve-roots,  and  in  some  cases 
true  gummatous  tumors  are  observed.  According  as  one 
or  the  other  feature  is  most  marked  the  disease  is  desig- 
nated as  syphilitic  meningomyelitis,  meningoneuritis,  or 
meningo-arteritis. 

The  symptoms  are  due  either  to  compression  or  directly 
to  the  diseased  condition  of  the  nervous  elements,  and  vary 
both  in  extent  and  intensity,  according  to  the  nature  and 
severity  of  the  primary  disease  :  Violent  paroxysms  of 


Fig.  27. 


COMPRESSION  MYELITIS.  169 

pain  ;  spastic  paraparesis  of  the  legs,  not  infrequently  more 
pronounced  on  one  side,  thus  pointing  to  a  unilateral 
lesion,  with  exaggerated  tendon  reflex  ;  vesical  and  rectal 
disturbances  (retention)  and  slight  sensory  disturbances 
(paresthesia). 

Diagnosis. — The  intermittence  of  the  symptoms  and 
the  occurrence  of  temporary  imj)rovement,  followed  by 
relapses,  are  characteristic  of  the  disease.  In  some  cases 
the  presence  of  brain  symptoms  may  assist  the  diagnosis 
(basal  palsies).  The  essential  point  in  the  diagnosis  is  the 
demonstration  of  a  previous  infection.  A  special  form  of 
this  disease  is  Erb's  syphilitic  spinal  paralysis.  This  is 
characterized  by  the  gradual  development  of  spastic  paresis 
in  the  legs,  with  slight  muscular  spasms,  increased  reflexes, 
mild  sensory  disturbances,  and  the  absence  of  ataxia  and  of 
pupillary  anomalies. 

Treatment. — Antisyphilitic  treatment  is  indicated  when 
there  is  the  slightest  suspicion  of  syphilis — inunctions,  in- 
jections, potassium  iodid.  If,  as  is  frequently  the  case, 
degenerative  processes  have  already  made  their  appear- 
ance, partial  improvement  is  all  that  can  be  expected, 
and  the  treatment  is  then  merely  symptomatic — baths, 
etc. 

3.  Compression  of  the  Spinal  Cord  (Compression 
Myelitis). — Although  this  may  be  due  to  a  variety  of  pro- 
cesses, it  seems  advisable  to  discuss  it  in  this  connection. 
In  many  cases  the  most  definite  diagnosis  that  can  be  made 
is  that  of  the  existence  of  compression  from  some  unknown 
cause. 

Compression  of  the  spinal  cord  may  be  due  to  : 

1.  Diseases  of  the  bone — caries  of  the  vertebrae,  com- 
pression by  a  purulent  focus,  exuberant  granulations 
pressing  on  the  meninges  (tubercular  meningitis),  seques- 
tra, fractures  of  the  bone  due  to  angulation  of  the  vertebral 
column,  carcinoma  beginning  in  the  vertebra,  and  trau- 
matic fractures  and  luxations  of  the  vertebral  column. 

2.  Diseases  of  the  meninges — pachymeningitis,  syphi- 


no  SPECIAL  PATHOLOGY  AND  TREATMENT. 

litic  meningitis,  tubercular  meningitis,  sarcoma,  lipoma, 
fibroma,  echinococcus. 

3.  Diseases  of  the  spinal  cord — glioma,  sarcoma,  gumma, 
tubercle. 

By  far  the  most  common  causes  of  compression  are 
caries  and  carcinoma.  As  a  result  of  the  compression  the 
integrity  of  the  nerve-fibers  and  nerve-cells  which  make 
up  the  corresponding  segment  is  seriously  impaired.  The 
first  effect  is  edema  in  the  segment  pressed  upon  (obstruc- 
tion of  the  lymph-channels)  ;  during  this  stage  there  is  a 
possibility  of  regeneration.  If,  however,  the  pressure  con- 
tinues and  increases  in  intensity,  the  nervous  elements 
become  swollen  and  soften  and  are  finally  completely 
destroyed.  In  most  cases,  therefore,  there  is  no  true 
myelitis. 

Course. — The  most  important  symptoms  of  compression 
are  the  violent  radiating  pains,  due  probably  to  irritation 
of  the  nerve-roots,  which  frequently  follow  the  distribution 
of  the  peripheral  nerves  (neuralgic  form),  and  either  sur- 
round the  trunk  like  a  girdle,  girdle  pains,  or  radiate  into 
the  extremities.  They  frequently  produce  reflex  con- 
tractions in  the  muscles  of  the  extremities,  as  these  are  no 
longer  under  the  control  of  the  will.  Hyperesthesia  and 
paresthesia  may  also  be  produced.  The  rigidity  in  the 
muscles  of  the  back  of  the  neck  and  back  must  also  be 
attributed  to  irritation  of  the  nerve-roots.  The  remaining 
symptoms  vary  according  as  the  lesion  is  situated  in  the 
cervical,  thoracic,  lumbar,  or  sacral  portion  of  the  cord  or 
in  the  cauda  equina.  (See  Part  IV,  3.)  They  consist, 
therefore,  of  palsies,  either  spastic  or  flaccid,  muscular 
atrophies,  and  disturbances  of  the  bladder  and  of  sensibil- 
ity. The  compression  usually  affects  the  thoracic  portion 
of  the  cord  (spastic  paraplegia  of  the  legs,  disturbances  of 
the  bladder  and  of  sensation  ;  the  arms  escape).  Death 
is  caused  by  the  primary  disease,  cystitis,  asthenia,  or 
decubitus. 

Diagnosis. — The  existence  of  compression   must  first 


COMPRESSION  MYELITIS.  171 

be  diagnosticated  and  then  its  level  (see  Part  IV,  3),  and 
to  do  this  it  is  best  to  proceed  in  the  following  manner  : 

First  determine  which  extremities  are  paralyzed — if  the 
legs  alone,  investigate  the  condition  of  the  knee-jerk. 
If  this  is  lost,  the  lesion  is  usually  situated  in  the  lumbar 
enlargement,  or  possibly  in  the  nerve-roots  contained  in 
the  Cauda  equina  (?) ;  if  fibers  of  the  sciatic  only  are  com- 
pressed, the  patellar  reflex  is  preserved.  If  the  knee- 
jerk  is  exaggerated,  the  lesion  must  be  situated  above  the 
reflex  arc — that  is,  either  in  the  thoracic  or  in  the  cervical 
portion  of  the  cord. 

If  the  arms  are  free  from  symptoms,  especially  if  the 
muscles  of  the  hands  are  not  atrophied,  the  lesion  is  sitii- 
ated  in  the  thoracic  portion  of  the  cord. 

Tumors  in  the  cauda  equina  produce  deep  sacral  pain, 
at  first  often  mistaken  for  sciatica,  vesical  and  rectal  par- 
alysis, disturbances  in  erection  and  ejaculation,  paraplegia 
dolorosa  inferior,  muscular  atrophies,  anesthesia  of  the 
legs  (especially  the  posterior  surface),  of  the  anal  region, 
and  of  the  scrotum  ;  decubitus.  The  lesion  may  be  more 
accurately  located  by  noting  which  muscles  are  atrophied 
(RD),  as  shown  in  Figure  17,  and  by  noting  the  level 
at  which  the  sensory  disturbance  begins.  Usually  the 
lesion  is  located  too  low,  because  we  are  not  as  yet  suf- 
ficiently informed  as  to  the  exact  localization  in  the  indi- 
vidual segments.  Tumors  especially  are  usually  found 
to  be  situated  two  or  three  segments  higher  than  would 
appear  to  be  indicated  by  the  level  of  the  highest  sensory 
disturbance. 

After  the  level  of  the  lesion  has  been  determined  as 
accurately  as  possible  by  a  process  of  exclusion  from 
below  upward,  and  from  above  downward,  we  determine, 
by  means  of  Plate  27,  which  spinal  process  or  processes 
correspond  to  the  level  found.  The  vertebral  column  is 
then  examined  with  special  care  in  this  region,  especially 
in  regard  to  its  mobility. 

In  determining  the  nature  of  the  compressing  process 


172  SPECIA  L  PA  THOLOG  Y  A  ND  TEE  A  TMENT. 

the  following  possibilities  must  be  taken  into  considera- 
tion : 

Caries. — Age  ;  changes  in  the  vertebral  column  (acute- 
angled  kyphosis)  ;  tenderness  on  pressure  ;  deep  abscesses  ; 
fever  (cystitis  being  excluded) ;  tuberculosis  in  other  parts 
of  the  body  ;  long  duration. 

Carcinoma. — Advanced  age  ;  cachexia  ;  metastasis,  rapid 
course  ;  most  intense  pain. 

Glioma  Medullare. — Slow  development,  the  symptoms 
at  first  unilateral. 

Even  after  the  most  careful  study  it  is  not  infrequently 
impossible  to  arrive  at  a  definite  diagnosis ;  compression 
may  be  absent,  even  in  spite  of  the  most  pronounced  symp- 
toms. 

Treatment. — In  caries,  extension  and  plaster-of-Paris 
jacket ;  arsenic  (operative  (?)  :  resection  of  the  vertebral 
arches).  In  tumors,  surgical  treatment.  Tumors  in  the 
Cauda  equina  give  the  best  prospects  of  success.  (See 
General  Treatment.)  In  most  cases  the  treatment  is 
symptomatic — cleanliness,  care  of  the  skin,  catheterization, 
morphin. 

4.  Acute  and  Chronic  Myelitis. — A  number  of  affec- 
tions differing  both  in  their  etiology  and  morbid  anatomy 
are  included  under  the  term  myelitis. 

They  are  all  characterized  by  a  diffuse  circumscribed  or 
cylindric  degeneration  of  nerve-fibers  and  cells  contained 
in  a  certain  region  of  the  spinal  cord,  by  the  formation  of 
neurogliar  tissue,  and  by  more  or  less  round-celled  infil- 
tration and  alteration  of  the  pia-arachnoid.  They  are 
usually  of  toxic  origin,  and  follow  in  the  wake  of  infectious 
diseases  (typhoid,  influenza,  gonorrhea,  erysipelas,  syphilis, 
etc.) ;  some  forms  are  due  to  direct  infection. 

They  are  classified,  according  to  their  clinical  course, 
into  acute,  lasting  several  weeks ;  subacute,  lasting  two  or 
three  months ;  and  chronic  forms.  The  commonest  seat 
of  myelitis  is  the  thoracic  portion  of  the  cord.  The  most 
frequent  form  is  that  due  to  syphilitic  infection. 


CHRONIC  MYELITIS.  1 73 

The  symptoms  vary  greatly  according  to  the  seat  of 
the  disease.     (See  Part  IV,  3.) 

Thoracic  myelitis,  the  most  frequent  form,  is  character- 
ized by  spastic  paraplegia  of  the  legs,  without  very  marked 
paroxysms  of  pain,  although  such  may  be  present ;  dis- 
turbances of  sensation  and  of  the  bladder  ;  paresthesia  and 
ataxic  conditions  in  the  legs. 

In  lumbar  myelitis  we  have  flaccid  paraplegia  of  the 
legs,  loss  of  reflexes,  paralysis  of  the  bladder,  etc. 

In  cervical  myelitis  there  are  spastic  paraplegia  of  the 
legs,  atrophy  of  the  muscles  of  the  arms,  etc. 

Decubitus  and  cystitis  frequently  mark  the  beginning  of 
the  end. 

This  disease  must  be  differentiated  from  compression 
myelitis  (g.  v.)  and  combined  system  diseases  (slow  course). 

The  method  of  determining  the  level  of  the  lesion 
and  the  treatment  will  be  found  under  Compression 
Myelitis. 

If  syphilis  is  present,  inunctions  are  indicated.  As  the 
degenerative  process  has  already  begun,  the  treatment  is 
only  partially  successful. 

Among  special  forms  should  be  mentioned  : 

(a)  Acute  disseminated  myelitis  (the  sudden  appearance 
of  multiple  foci  of  degeneration  in  the  white  substance), 
which  is  again  subdivided  into  an  ataxic  and  a  paraplegic 
form.  The  ataxia  is  not  accompanied  by  nystagmus,  thus 
differentiating  the  disease  from  sclerosis.  Disturbance  of 
the  speech  and  psychic  disturbances  are  often  present. 
This  form  often  occurs  in  association  with  optic  neuritis, 
resembling  in  this  respect  multiple  sclerosis,  which  runs  a 
more  chronic  course.  The  condition  is  then  termed  dis- 
seminated encephalomyelitis.  When  it  occurs  in  associa- 
tion with  multiple  neuritis,  we  speak  of  disseminated  neu- 
romyelitis. 

(6)  In  severe  anemias  numerous  foci  of  degeneration  are 
found,  especially  in  the  posterior  and  lateral  columns. 
The  condition   is    probably  secondary  to  disease  of  the 


174  S  FECI  A  L  PA  THOLOG  Y  A  ND  TEE  A  TMENT. 

blood-vessels,  as  are  also,  in  some  instauees,  some  of  the 
above-mentioned  forms. 

The  symptoms  are  mild  ataxia  and  sensory  disturbances 
and  loss  of  patellar  reflex. 

5.  Syringomyelia. — This  term  is  applied  to  focal  dis- 
eases characterized  by  abnormal  cavity  formations  in  the 
interior  of  the  white  substiince.  The  condition  may  be 
due  to  various  causes  ;  it  may  be  congenital  or  may  develop 
later  in  life  in  predisposed  individuals  (hydromyelia).  It 
may  be  due  to  the  breaking-down  of  central  proliferations 
of  neurogliar  tissue  (central  gliosis),  or  may  occur  from 
some  unknown  cause  after  trauma,  hemorrhages,  etc. 

The  excavations  may  include  the  entire  length  of  the 
spinal  cord,  and  may  even  extend  into  the  medulla  oblon- 
gata. The  favorite  seat  is  the  cervical  enlargement,  so  that 
the  principal  symptoms  are  those  produced  by  a  lesion  of 
this  portion  of  the  cord. 

The  cavity  usually  begins  in  the  vicinity  of  the  central 
canal,  and  leads  to  gradual  destruction  of  the  central  gray 
substance  in  the  anterior  and  posterior  horns,  and  of  the 
nerve-fibers  and  ganglion  cells  situated  in  those  regions. 

The  individual  symptoms  taken  by  themselves  are  not 
characteristic,  but  taken  altogether  they  are  practically 
pathognomonic  of  syringomyelia.     They  are  : 

1,  Progressive  muscular  atrophy  and  paralysis,  affecting 
chiefly  the  upper  extremities,  more  pronounced  on  one  side, 
sometimes  more  bilateral  in  character.  The  small  muscles 
of  the  hand  and  the  triceps  are  most  frequently  attacked  ; 
the  atrophied  muscles  are  the  seat  of  fibrillar  contractions 
and  give  the  reactions  of  degenerations  (degenerative 
atrophy,  disease  of  the  peripheral  neuron  cells). 

2.  Disturbances  of  sensation  in  the  arms,  especially  anal- 
gesia and  thermo-anesthesia,  with  integrity  of  the  tactile 
sense  (dissociation  of  the  anesthesia). 

S.  Trophic  disturbances  in  the  fingers  and  joints,  such  as 
necrosis,  suppuration,  subluxations,  hypertrophies. 

In  addition  there  may  be  spastic  paraparesis  of  the  legs 


MULTIPLE  SCLEROSIS.  175 

or  bulbar  symptoms  (paralysis  of  the  spinal  accessory, 
hypoglossus,  etc.).  Atypical  cases  resembling  tabes,  spastic 
spinal  paralysis,  etc.,  are  not  infrequently  observed. 

The  process  is  slowly  progressive. 

Diagnosis. — Spinal  muscular  atrophy,  in  which  sensa- 
tion is  normal,  nmst  be  excluded.  Atypical  cases  are  very 
difficult  to  recognize. 

Treatment. — Symptomatic  ;  electricity,  baths,  etc. 

6.  Hemorrhages  in  the  Central  Canal. — Hemorrhage 
may  be  either  extramedullary  and  between  the  meninges 
(intrameningeal  apoplexies,  hematorrhachis),  or  in  the  sub- 
stance of  the  spinal  cord  itself  (hematomyelia).  They  are 
usually  due  to  traumatism.  In  intrameningeal  hemorrhage 
the  symptoms  are  similar  to  those  produced  by  spinal 
meningitis,  except  that  the  phenomenon  occurs  suddenly 
after  trauma  (symptoms  of  irritation  of  the  roots,  para- 
plegia, disturbances  of  the  bladder  and  of  sensation). 

The  symptoms  of  hematomyelia  present  the  same  com- 
binations as  those  in  syringomyelia  ;  the  localization  is  the 
same,  but  they  appear  suddenly  after  trauma  and  vary 
somewhat  according  to  the  seat  and  extent  of  the  lesion. 
The  seat  of  the  hemorrhage  is  determined  by  the  princi- 
ples laid  down  on  page  171. 

The  condition  is  not  infrequently  improved  by  treat- 
ment, which  consists  of  rest  and,  later,  warm  baths. 

7.  Multiple  Cerebrospinal  Sclerosis  (Sclerose  en 
plaques). — Focal  sclerosis  is  a  disease  of  the  most  enig- 
matic character.  It  is  characterized  by  the  appearance  of 
a  number  of  small,  irregularly  scattered  foci  in  the  brain 
and  spinal  cord  (primarily  encephalitic  or  myelitic  ?),  with 
destruction  of  the  medullary  sheath  of  the  nerve-fibers 
situated  in  those  foci.  The  axis-cylinder,  however,  per- 
sists and  continues  to  functionate  for  some  time  longer,  so 
that  the  fibers  are  not  completely  destroyed.  The  disease 
frequently  occurs  in  young  subjects  in  the  wake  of  infec- 
tious diseases  (?). 

The  symptoms  are  progressive  and  develop  very  grad- 


176  SPECIAL  PA  THOLOG Y  AND  TEEA  TMENT. 

ually.  In  the  beginning  the  patient  experiences  difficulty 
in  performing  certain  movements.  There  are  weakness 
and  want  of  control  of  the  arms  and  legs,  tremors  ap- 
pear when  the  patient  takes  hold  of  an  object  (intention 
tremor),  and  the  gait  becomes  stiff  and  uncertain  (spastic 
and  ataxic). 

In  addition  nystagmus,  scanning  speech,  slight  vesical 
disturbances,  and  occasionally  optic  atrophy  develop. 
The  knee-jerks  are  exaggerated.  From  time  to  time  there 
are  apoplectiform  attacks  ;  sensory  disturbances  are  usu- 
ally slight ;  paresthesia  may  be  present. 

While  this  description  applies  to  typical  cases,  there 
are  many  variations,  depending  on  the  site  of  the  focus,  and 
these  formes  fi-usfes  (spurious  forms)  of  multiple  sclerosis 
are  frequently  mistaken  for  other  diseases.  Many  of  the 
above-named  symptoms  may  be  absent.  In  some  cases 
ataxia  is  more  marked,  in  others  the  spastic  paralysis  of 
the  legs  ;  a  third  group  is  characterized  by  the  presence 
of  bulbar  symptoms. 

Course. — The  course  of  the  disease  is  extremely  chronic 
and  occasionally  interrupted  by  teniporary  improvement. 
The  intelligence  may  eventually  be  affected. 

Diagnosis. — We  must  exclude  neurasthenia,  hysteria 
(occasional  presence  of  different  clinical  pictures),  para- 
lytic dementia  (pupils,  history).  Other  diseases  of  the 
spinal  cord,  such  as  myelitis,  spastic  spinal  paralysis,  etc., 
can  not  always  be  excluded  with  certainty. 

Treatment.  —  Gymnastic  exercises,  massage,  baths, 
symptomatic. 

B.  SYSTEM  DISEASES. 

For  a  description  of  their  general  characters  see  Part 
IV,  3,  page  104.  They  are  for  the  most  part  very  chronic, 
progressive,  and  incurable,  because  when  cells  and  fibers 
once  degenerate  in  the  brain  and  spinal  cord,  they  can 
never  recover. 

8.  Spastic  Spinal  Paralysis. — This  is  a  rare  disease. 


AMYOTROPHIC  LATERAL  SCLEROSIS.  177 

The  anatomic  basis  is  a  symmetric  primary  degeneration 
of  the  pyramidal  tract  (central  motor  neuron  complex). 

Course. — The  disease  begins  in  adults  (children  ?)  with 
a  slowly  progressive  spastic  paralysis  of  the  legs,  arms, 
and  facial  muscles,  without  muscular  atrophy  or  distur- 
bance of  the  bladder  or  of  sensation.  The  knee-jerks  and 
ankle-clonus  are  exaggerated. 

There  are  also  other  forms  of  spastic  bilateral  palsies ; 
the  cerebral-  spastic  paralysis  of  childreUy  the  form  occurring 
in  multiple  sclerosis,  hydrocephalus,  myelitis,  etc.  In  most, 
but  not  all,  of  these  cases  other  symptoms  are  superadded 
to  those  mentioned  above  (impure  cases). 

9.  Amyotrophic  Lateral  Sclerosis. — In  addition  to 
the  pyramidal  tract  the  motor  cells  in  the  anterior  horn 
(peripheral  neuron),  especially  in  the  lumbar  enlargement 
and  possibly  also  in  the  nerve  nuclei  of  the  bulb,  are  in- 
cluded in  the  morbid  process.     (See  Part  IV,  3.) 

Course. — The  disease  begins  in  adults  with  the  appear- 
ance of  muscular  weakness  and  atrophy  in  the  hands  (inter- 
ossei,  thenar  muscles),  accompanied  or  followed  later  by 
the  development  of  a  spastic  paretic  gait.  The  atrophy  of 
the  muscles  of  the  arm  slowly  progresses  (see  under  Spinal 
Muscular  Atrophy),  the  muscles  present  fibrillary  contrac- 
tions and  the  reactions  of  degeneration.  Eventually  the 
muscles  of  the  arm  and  shoulder  atrophy  completely.  The 
reflexes  are  preserved  or  even  exaggerated  ;  the  legs  are 
completely  paralyzed  and  spastic ;  the  knee-jerks  are  exag- 
gerated ;  ankle-clonus  is  present ;  bladder  and  sensation  are 
normal;  pain  is  present,  especially  in  the  muscles  of  the 
arm.  In  many  instances  the  symptoms  of  chronic  progres- 
sive bulbar  paralysis  are  superadded  early  in  the  course  of 
the  disease. 

Treatment. — Symptomatic;  electricity,  baths,  arsenic, 
strychnin,  feeding  by  means  of  esophageal  tube. 

10.  Progressive  Spinal  Muscular  Atrophy. — In  this 
affection  the  motor  ganglion  cells  in  the  anterior  horn  of 
the  spinal  cord,  especially  in  the  cervical  enlargement,  are 

12  ' 


178  SPECIAL  PA  THOLOG  Y  AND  THE  A  TMENT. 

destroyed  by  a  slowly  progressive  degeneration.  The  pyr- 
amidal tract  is  not  involved.  The  alterations  in  the  muscle 
consist  in  a  slow,  degenerative  atrophy  of  the  individual 
fibrils.  There  is  an  increase  in  the  number  of  nuclei  in 
the  sheath  of  the  fibrils  and  the  protoplasm  shrinks, 
although  even  very  much  attenuated  fibers  may  show  a 
distinct  transverse  striation.  Eventually  the  sheath  disap- 
pears along  with  the  remains  of  the  protoplasm,  and 
nothing  remains  but  the  connective-tissue  portion  of  the 
fiber. 

Course. — The  clinical  symptoms  are  those  of  amyo- 
trophic lateral  sclerosis  without  spastic  phenomena  :  A  very 
slowly  developing  and  gradually  extending  atrophy  and 
paralysis  of  the  small  muscles  of  the  hand  and  later  of  all 
the  nmscles  of  the  arm  and  shoulder,  with  fibrillary  con- 
tractions and  the  reactions  of  degeneration ;  the  legs  often 
escape ;  sensation  and  bladder  function  are  not  affected. 
Duration,  one  to  several  years.  Owing  to  the  atrophy  of 
the  thenar  muscles  adduction  of  the  thumb  is  impossible — 
Simian  hand.  The  deltoid  muscle  often  atrophies  before 
the  other  muscles  of  the  arm  and  forearm.  Even  the 
nuchal  muscles  and  the  intercostals,  or  rarely  the  dia- 
phragm, may  be  involved.  Bulbar  paralysis  may  follow 
or  may  develop  simultaneously. 

Diagnosis. —  See  under  Progressive  Muscular  Dys- 
trophy. 

Treatment. — See  Amyotrophic  Lateral  Sclerosis. 

There  is  another  form  of  muscular  atrophy,  the  so-called 
peroneal  type  of  progressive  muscular  atrophy.  This  form 
may  occur  in  several  members  of  the  same  family,  and  is 
characterized  by  atrophy  of  the  peronei  and  tibialis  anticus, 
etc.,  in  addition  to  the  small  muscles  of  the  hand.  The 
condition  leads  to  paralytic  club-foot  and  peroneal  gait,  in 
which  the  patient  raises  the  thighs  unusually  high,  while 
the  tip  of  the  foot  drags  on  the  ground.  The  patellar 
reflexes  are  abolished.  Slight  disturbances  of  sensibility 
are  present  in  the  toes  and  fingers.     The  atrophy  in  the 


PROGRESSIVE  MUSCULAR  DYSTROPHY.  179 

muscles  of  the  arms  and  legs  gradually  increases.  Ana- 
tomically, we  find  degenerative  changes  in  the  peroneal, 
median,  and  thenar  nerves  and  in  the  lumbar  and  cervical 
enlargement,  where  the  cells  of  the  anterior  horns  appear 
to  be  involved. 

II.  Progressive  Muscular  Dystrophy  (Primary 
Myopathy). — Whether  this  disease  is  of  spinal  origin  is 
still  an  open  question,  as  up  to  the  present  time  the  changes 
found  have  been  confined  to  the  muscles.  It  is  to  be 
regarded  as  the  last  link  in  the  chain  of  motor  system 
diseases. 

The  muscle-fibers  undergo  an  extremely  gradual,  non- 
degenerative  atrophy.  The  individual  fibers  shrink  and 
eventually  disappear ;  the  transverse  striations  persist  for 
a  long  time ;  the  muscular  nuclei  become  multiplied,  fat  is 
deposited  between  the  fibers,  and  hypertrophic  fibers  are 
not  uncommon.  Their  thickness  measures  from  150  to 
200  11.  The  disease  is  often  hereditary  and  makes  its 
appearance  in  early  life.  The  atrophied  muscles  present 
the  phenomenon  of  simple  atrophy  only  ;  fibrillary  con- 
tractions and  the  reactions  of  degeneration  are  absent ;  the 
atrophy  is  slowly  progressive.  Recovery  does  not  occur, 
but  the  process  is  sometimes  brought  to  a  standstill. 

Depending  on  the  period  when  the  disease  first  makes 
its  appearance,  various  forms  are  distinguished,  which  in 
their  subsequent  course  merge  into  one  another.     They  are  : 

(a)  Pseudohypertrophy. — This  begins  in  early  child- 
hood, with  weakness  in  the  muscles  of  the  back,  gradually 
extending  to  the  lumbar  and  femoral  muscles.  The  muscles 
show  no  alteration  in  shape.  They  appear  rather  hyper- 
trophic on  account  of  the  deposition  of  fat  (lipomatosis). 
The  children  are  unable  to  get  up  from  the  floor  without 
supporting  themselves  with  their  hands  ;  the  gait  becomes 
waddling,  and  finally  walking  is  impossible.  Later  curva- 
ture of  the  spine  develops  (lordosis). 

(b)  The  Infantile  Variety. — This  begins  in  children, 
frequently  with  atrophy  and  paralysis  of  the  facial  muscles 


180  SPECIAL  PATHOLOGY  AND  TREATMENT. 

(expressionless  countenance  —  ^'  facies  myopathique  "). 
Later  the  muscular  atrophies  of  the  extremities  belonging 
to  the  next  form  are  superadded. 

(c)  Juvenile  Form. — Tliis  appears  during  or  after 
puberty.  We  distinguish  a  shoidder-girdle  type,  aifecting 
the  pectoral  muscles,  trapezius,  latissimus  dorsi,  serratus 
anticus,  triceps,  and  biceps,  which  undergo  atrophy  in  the 
order  named.  The  small  muscles  of  the  hand,  the  deltoid, 
and  the  sternocleidomastoid  escape  (the  opposite  condition 
obtains  in  spinal  muscular  atrophy).  The  other  is  a  pelvic 
girdle  type,  in  which  the  quadriceps,  glutei,  and  peronei 
are  affected.  The  calf  muscles  escape.  The  two  forms 
merge  into  one  another  or  exist  side  by  side. 

The  diagnosis  of  muscular  atrophies  requires  a  famili- 
arity with  the  normal  configuration  of  the  extremities.  A 
practised  eye  will  recognize  at  the  first  glance  atrophy  of 
the  lumbricales  by  the  depressions  between  the  first 
phalanges,  of  the  thenar  and  hypothenar  groups  by  ab- 
normal dimples,  of  the  pectoral  muscles  by  deep  depres- 
sion below  the  clavicle,  which  is  very  prominent,  of  the 
deltoid  by  flattening  of  the  shoulder,  of  the  trapezius  by 
diminution  in  the  size  of  the  neck,  of  the  rhomboid 
muscles  by  the  presence  of  abnormal  depressions  where 
normally  elevations  should  exist,  of  the  quadriceps  by  a 
flattening  of  the  upper  surface  of  the  thighs,  or  of  the 
peronei  by  the  absence  of  normal  prominence  outward 
from  the  crest  of  the  tibia,  etc. 

The  differential  diagnosis  between  the  individual  forms 
is  very  simple.  It  is  based  purely  on  the  beginning  of 
the  disease. 

Treatment. — Symptomatic  and  orthopedic. 

12.  Anterior  Poliomyelitis. — The  inflammatory  dis- 
eases of  the  gray  substance  in  the  anterior  horn  of  the 
spinal  cord  are  either  acute  or  chronic,  and  exert  their 
malign  influence  on  the  motor  ganglion  cells  situated  in 
the  region.  Accordingly  they  lead  to  degenerative  mus- 
cular atrophies  and  paralyses. 


ANTERIOR  POLIOMYELITIS.  181 

(a)  Acute  Anterior  Poliomyelitis. — This  affection 
makes  its  appearance  during  the  first  years  of  life,  rarely 
in  adult  age,  as  an  acute  infectious  disease,  the  bacterial 
origin  of  which  is  unknown.  It  manifests  itself  in  an 
inflammation  of  the  substance  of  the  anterior  horns,  the 
inflammation  beginning  in  the  blood-vessels.  The  disease 
is  ushered  in  by  fever,  vomiting,  and  delirium.  This  is 
followed  by  moderately  deep  coma,  lasting  several  days, 
after  which  the  patient  improves,  but  there  is  found  to  be 


Fig.  28. — Transverse  section  of  the  lumbar  enlargement  in  ante- 
rior poliomyelitis.  The  diseased  focus  is  readily  seen  in  the  anterior 
horn,  especially  in  the  lateral  cell-groups.  The  entire  right  half  of 
the  cord  is  shrunken. 


a  flaccid  paralysis  of  the  arms  and  legs  (rarely  of  the  face, 
etc.)  and  of  the  bladder,  with  loss  of  reflexes,  but  without 
pain  or  sensory  disturbances.  Some  of  the  paralytic 
phenomena  disappear  after  a  time  ;  others  are  permanent, 
but  are  usually  confined  to  one  side.  The  affected  muscles 
undergo  a  rapid  degenerative  process. 

The  remains  of  this  disease  which  persist  in  later  life 
are  termed  infantile  spinal  paralysis.  Their  anatomic  basis 
consists  in  a  shrinking  of  the  affected  anterior  horn.     (See 


182  SPECIAL   PATHOLOGY  AND   TREATMENT. 

Fig.  28,  anterior  horn  on  the  right  side.)  Contractures 
result  from  the  action  of  the  antagonistic  muscles ;  the 
development  of  the  affected  members  is  retarded. 

The  most  frequent  palsies  that  result  are  paralysis  of 
the  peronei  and  extensors  (talipes  equinovarus),  paralysis 
of  the  upper-arm  type  (deltoid,  biceps,  brachialis  anticus, 
supinator  longus),  and  of  the  forearm  type  (triceps,  exten- 
sors of  the  hand). 

Treatment. — In  the  beginning,  rest,  baths,  leeches  to 
the  back,  purgatives,  and  sweat  cures ;  later,  gymnastic 
exercises  and  orthopedic  treatment. 

An  important  orthopedic  measure  consists  in  trans- 
ferring the  action  of  an  adjoining  sound  muscle  to  the 
tendon  of  the  paralyzed  muscle.  In  talipes  valgus  the 
extensor  hallucis  is  sutured  to  the  tendon  of  the  tibialis 
anticus;  in  talipes  varus  the  hallucis  is  attached  to  the 
extensor  digitorum  communis  ;  in  pes  equinus  the  peroneus 
and  flexor  digitorum  to  the  tendo  Achilles,  etc.  Good  re- 
sults have  also  been  achieved  by  dividing  the  muscles.  In 
the  forearm  the  thenar  and  radial  muscles  can  be  advan- 
tageously utilized  to  supply  the  function  of  the  paralyzed 
flexors  and  extensors  of  the  fingers. 

(b)  Chronic  Poliomyelitis. — So-called  chronic  atrophic 
spinal  paralysis  is  a  rare  disease,  occurring  in  adults, 
characterized  by  the  more  or  less  rapid  development  of 
flaccid  paralysis,  first  in  the  lower,  and  later  in  the  upper, 
extremity,  followed  by  degenerative  atrophy.  The  reflexes 
are  abolished  ;  sensation  and  bladder  function  are  normal. 
Many  muscles  may  escape  ;  improvement  is  possible. 

Diagnosis. — Lumbar  myelitis,  sensory  disturbances, 
and  multiple  neuritis  (g.  v.)  must  be  excluded. 

Treatment. — Baths,  electricity,  symptomatic. 

13.  Tabes  Dorsalis. — The  anatomic  basis  of  tabes  dor- 
salis  consists  in  a  chronic  progressive  degeneration  of  the 
peripheral  sensory  neuron  complex,  especially  of  the  lower 
extremities.  The  degeneration  aflects  most  extensively 
that  portion  of  the  neuron  complex  which  begins  in  the 


TABES  DOMSALIS.  183 

spinal  ganglia,  enters  the  substance  of  the  spinal  cord 
through  the  posterior  roots,  and  continues  \vithin  the  cord 
(the  long  tracts  in  the  posterior  columns  ;  the  short  tracts 
enter  the  posterior  horns,  Clarke's  columns,  and  anterior 
horns  ;  see  p.  51).  The  peripheral  portions  of  the  neuron, 
consisting  of  tlie  sensory  cutaneous  nerves,  are,  however, 
attacked  by  degenerative  processes.  But  in  addition  to 
these  tracts  the  tabetic  process  frequently  attacks  other 
pathways,  both  sensory  (central)  and  motor  (peripheral  and 
central  neuron  complexes),  producing  combined  forms.  In 
typical  cases  certain  definite  reflex  arcs  (reflex  collaterals) 
— namely,  those  concerned  in  the  patellar  and  pupillary 
reflexes — are  first  destroyed.  It  is  not  as  yet  definitely 
known  at  what  point  the  disease  takes  its  origin.  (For 
further  details  of  the  morbid  anatomy  the  student  is 
referred  to  Plates  77  and  78.) 

As  has  been  stated,  the  peripheral  neuron  complex  of 
the  lower  extremities  is  most  frequently  attacked,  more 
rarely  that  of  the  upper  extremity  only  is  affected  (high 
tabes),  either  alone  or  in  combination  with  the  peripheral 
neuron  of  the  fifth  nerve,  especially  the  descending  root 
of  the  glossopharyngeal,  etc.  These  forms  are  all  to  be 
regarded  as  different  varieties  of  the  same  disease. 

In  a  large  proportion  of  cases  a  former  syphilitic  in- 
fection is  shown  by  statistics  to  be  the  cause  of  the  degen- 
erative process. 

The  symptoms  develop  slowly  and  may  be  divided  into 
three  stages  : 

1.  The  Neuralgic  Stage. — This  is  characterized  by 
violent,  fulminating  attacks  of  pain,  with  occasional  exacer- 
bations, radiating  into  the  legs  (lancinating  pains,  symp- 
toms of  irritation  of  the  posterior  roots  ?),  and  not  infre- 
quently by  paresthesias  and  painful,  oppressive  sensations 
in  the  epigastric  region  (girdle  pain).  If  the  patient  pre- 
sents himself  at  this  time,  the  examiner,  as  a  rule,  finds 
the  two  symptoms,  which,  when  present  together,  are 
pathognomonic  of  tabes  ;  they  are  : 


184  SPECIAL  PATHOLOGY  AND  TREATMENT. 

1.  Reflex  pupillary  rigidity ,  or  failure  to  react  to  light 
with  accommodation  preserved  ;  contracted  pupil. 

2.  Loss  of  the  patellar  reflex  (WestphaPs  sign). 

2.  The  Ataxic  Stage. — This  may  make  its  appearance 
after  a  variable  interval  (sometimes  lasting  many  years) 
has  elapsed  since  the  appearance  of  the  first  symptoms. 
The    most   characteristic   feature    is  the    tabetic   gait  or 


Fig.  29. — Oculomotor  nucleus  in  tabes  dorsalis  (medullary  sheath 
stain,  photograph,  magnified  80  times):  F,  Posterior  longitudinal 
bundle;  d',  dorsal,  y,  ventral,  c,  central,  x,  Westphal's,  nucleus,  which 
in  this  illustration  appears  unusually  pale,  owing  to  a  marked  degen- 
eration of  the  fibers  (connected  with  loss  of  the  pupillary  reflex?). 


ataxia.  The  patient  throws  his  feet  about  and  brings 
them  to  the  ground  with  a  stamp  ;  the  gait  is  uncertain, 
but  not  paretic.  The  ataxia  is  considerably  increased 
when  the  patient  closes  his  eyes  (Romberg's  phenome- 
non). 

In  addition  there  are  slight  disturbances  of  the  bladder 


HEREDITARY  ATAXIA.  185 

function,  the  sensitiveness  to  painful  and  thermic  stimuli  is 
blunted,  and  optic  atrophy  may  make  its  appearance. 

3.  Paralytic  Stage. — The  interval  between  this  and 
the  preceding  stage  is  also  variable.  The  ataxia  gradually 
increases,  and  can  even  be  noticed  as  the  patient  moves 
about  in  bed,  the  gait  becomes  more  and  more  paretic- 
ataxic,  and  finally  walking  becomes  impossible.  As  a 
rule,  there  is  never  a  true  paralysis. 

The  disturbances  of  sensation  and  of  the  bladder  func- 
tion increase. 

The  lancinating  pains  are  constantly  present  and  peri- 
odically culminate  in  the  so-called  tabetic  crises,  consisting 
in  intensely  painful  attacks  of  colic,  vomiting,  cough,  and 
dyspnea  (abdominal,  gastric,  laryngeal  crises,  etc.). 

Effusions  into  the  joints,  arthropathies  (trophic?),  and 
ulcerations  (inal perforant)  are  common.  Not  infrequently 
paralysis  of  the  eye  muscles  and  of  the  trifacial  nerve  and 
hemicrania-like  conditions  occur  early  in  the  disease. 

The  diagnosis  of  tabes  presents  no  difficulty  in  ordinary 
cases.  It  may,  however,  be  obscured  by  an  atypical  mode 
of  onset  and  by  the  absence  of  important  symptoms,  such 
as  the  pupillary  reflex,  and  the  abolition  of  the  patellar 
reflex.  Alcoholic  and  diabetic  neuritis  and  hereditary 
ataxia  must  be  excluded.  The  differential  diagnosis  from 
these  conditions  will  be  discussed  under  their  respective 
heads. 

Treatment. — The  value  of  antisyphilitic  treatment  is 
doubtful.  Baths,  rest,  massage,  gymnastic  exercises  to 
correct  the  muscular  incoordination,  attention  to  diet, 
electricity,  suspension  ;  nitrate  of  silver,  potassium  iodid, 
secale  cornutum,  antinervin,  narcotics. 

14.  Hereditary  Ataxia  (Friedreich's  Disease). — 
This  is  a  combined  system  disease.  The  degeneration  in 
the  posterior  columns  of  the  spinal  cord  is  accompanied 
by  a  similar  process  in  the  direct  cerebellar  tract  and 
pyramidal  tract..  The  cerebellum  is  probably  also  in- 
volved.    The  disease  often  appears  in  families. 


186     SPECIA L  PA  THOLOG  Y  AND  TBEA  TMENT. 

It  begins  in  early  life,  with  a  gradually  increasing  dis- 
turbance of  the  coordination  in  the  movements  and  attitude 
of  the  extremities,  trunk,  and  head  ;  ataxia  of  the  legs 
and  arms — Romberg^s  phenomenon.  The  incoordination 
manifests  itself  in  the  trunk,  both  on  motion  and  during 
rest,  as  when  the  patient  is  seated.  The  gait  is  vacillating, 
resembling  the  cerebellar  gait,  and  the  paresis  is  usually 
more  prominent.  In  addition  there  are  nystagmus,  slight 
disturbances  of  speech,  and  some  disturbance  of  sensibility 
and  of  the  bladder  function. 

Diagnosis. — The  knee-jerk  is  abolished,  but  the  pupil- 
lary reflex  is  normal— a  diiferential  point  in  the  diagnosis 
from  tabes.  The  neuralgic  pains  of  tabes  are  also  absent. 
The  disease  slowly  progresses  to  a  complete  paralysis ; 
contractures  in  the  fingers  are  common.  It  lasts  many 
years.     Recovery  has  never  been  reported. 

Treatment. — Symptomatic. 

Other  forms  of  combined  system  diseases  similar  to 
hereditary  ataxia  also  occur,  presenting  in  the  main  the 
symptoms  of  a  spastic  spinal  paralysis  with  some  distur- 
bance of  sensation  and  bladder  function,  combined  with 
ataxia.  This  class  includes  a  hereditary  form  of  spastic 
spinal  paralysis  affecting  the  pyramidal  tract,  posterior 
columns,  and  lateral  cerebellar  tract,  besides  other  varieties 
concerning  which  but  little  is  known. 

IV.  DISEASES  OF  THE  PERIPHERAL  NERVES. 

A.  DISEASES  OF  SINGLE  NERVES. 

A  great  variety  of  causes  may  produce  lesions  of  the 
peripheral  nerves :  Traumatism,  tumors  of  all  kinds 
(tumors  in  the  soft  parts,  small  exostoses  in  the  bony 
canals,  neuromata),  cicatricial  processes,  chemic  changes 
produced  by  the  formation  of  toxic  substances  during  the 
course  of,  or  subsequent  to,  acute  infectious  diseases  in 
which  individual  nerves  may  be  injured — toxic  neuritis. 
A  spontaneous  (inflammatory  ?)  affection  of  single  nerves — 


DISEASES  OF  THE  MOTOR  NERVES.  187 

rheumatic  neuritis — is  also  quite  common,  especially  facial 
neuritis. 

In  severe  neuritic  processes  the  nerve- fiber  is  com- 
pletely destroyed  and  replaced  by  sclerotic  connective 
tissue.  In  milder  grades  of  the  degenerative  processes 
the  nerves  may  be  completely  regenerated  (parenchyma- 
tous neuritis),  the  nerve  tissue  differing  in  this  respect 
from  the  tissues  of  the  spinal  cord.  We  distinguish 
various  forms  according  to  their  severity. 

I.  The  Diseases  of  the  Motor  Nerves. — Any  of 
the  above-mentioned  lesions  affecting  a  purely  motor  or 
mixed  nerve  may  give  rise  to  paralytic  and  irritative 
symptoms  (localized  muscular  spasms)  in  the  domain  of 
the  affected  nerve.  We  distinguish  three  forms  of  paral- 
ysis :  A  severe,  a  moderately  severe,  and  a  mild  form, 
depending  on  the  duration,  which  in  turn  depends  on  the 
severity  of  the  neuritic  process. 

For  the  details  in  the  diagnosis  the  student  is  referred 
to  the  paragraph  on  Electric  Diagnosis,  Part  IV,  page 
108. 

The  most  frequent  forms  of  paralysis  are  :  Facial  par- 
alysis— usually  rheumatic — in  middle-ear  disease,  due  to 
a  compression  neuritis  of  the  nerve  in  its  course  through 
the  bony  canal.  Paralysis  of  the  radial  nerve,  usually  due 
to  compression  and  occurring  especially  in  narcosis,  in  par- 
alysis of  the  fifth  and  sixth  roots  of  the  brachial  plexus, 
by  compression  between  the  clavicle  and  the  first  rib 
during  sleep,  and  in  lead-poisoning  ;  oculomotor  paralysis 
— postdiphtheric  ;  recurrens  paralysis,  due  to  compres- 
sion by  aneurysms  or  tumors ;  paralysis  of  the  spinal 
accessory ;  paralysis  of  the  brachial  plexus  during  labor ; 
paralysis  of  the  median  and  thenar  nerves  from  injuries. 

For  a  detailed  account  of  the  symptoms  of  these  and 
other  possible  paralyses  consult  Part  IV,  3,  page  97. 

Of  the  localized  muscular  spasms  produced  by  disease 
of  individual  peripheral  nerves  the  more  frequent  are  the 
following : 


188  SPJECIA  L  PA  THOLOG  Y  A ND  TBEA  TMENT. 

Spasm  of  the  facial  nerve,  clonic  convulsions  of  the 
entire  musculature  of  one  side  of  the  face  {tic  conmilsif). 
A  partial  form  is  represented  by  blepharospasm,  or  tonic 
and  clonic  convulsions  of  the  eyelids. 

Spasm  of  the  muscles  of  mastication,  or  trismus,  a 
tonic  spasm  usually  central  in  origin. 

Spasm  of  the  spinal  accessory, — spastic  torticollis, — 
a  severe  tonic  and  clonic  convulsion,  frequently  involving, 
in  addition  to  the  trapezius  and  sternocleidomastoid,  the 
other  nuchal  muscles  innervated  by  the  cervical  plexus 
(splenius,  etc.).  The  latter  group  may  also  be  attacked 
separately. 

Clonic  spasm  of  the  diaphragm,  singultus,  spasm 
of  the  calf  muscles  (crampus  sensu  strictiori),  and  others. 

The  cause  of  these  cramps  is  not  by  any  means  always 
a  lesion  of  the  peripheral  motor  nerves.  In  many  cases 
they  are  reflex  in  character,  as,  for  instance,  in  violent 
neuralgia,  etc. 

It  is  often  very  difficult  to  distinguish  convulsions  of 
central  (psychogenic)  origin  from  those  due  to  peripheral 
irritation.  The  two  causes  may  be  at  work  at  the  same 
time  and  together  produce  the  convulsions  (predisposition 
due  to  central  disease  and  peripheral  exciting  cause). 
The  spasms  that  are  to  be  interpreted  in  this  way  include 
fits  of  yawning,  laughing,  weeping,  and  shouting  (see  Hys- 
teria), the  saltatory  reflex  spasm  (muscular  contractions 
when  the  patient  attempts  to  walk),  multiple  paramyo- 
clonus (see  Hysteria),  also  the  so-called  occupation  neuroses 
which  occasionally  attack  neurasthenic  individuals  and 
consist  in  disturbances  of  the  coordination  of  certain 
muscles  required  for  definite  movements  performed  in  the 
course  of  the  patient's  ordinary  occupation,  especially  in 
manual  work  (reading,  sewing,  violin-  and  piano-playing, 
etc.). 

Writer's  cramp — mogigraphia — consists  in  uncontrol- 
lable spasms  in  the  muscles  of  the  hand  and  fingers, 
accompanied  by  tremors  and  weakness  and,  occasionally, 


DISEASES  OF  THE  SENSORY  NERVES.  189 

painful  sensations.  Continuous  writing  becomes  utterly 
impossible  (spastic  paralytic  tremor-like  neuralgic  form). 
The  disability  is  increased  by  psychic  emotion  and  fear, 
greatly  as  in  stammering. 

Treatment. — The  patient  must  stop  writing  at  stated 
intervals  and  use  a  thick  penholder  (Nussbaum's  holder). 
Cold  sponging,  massage,  gymnastic  exercises,  electric  treat- 
ment, bending  of  the  arms,  writing  machine. 

Note. — Occupation  palsies  similar  to  the  occupation  spasms  and 
also  associated  with  muscular  atrophy  are  sometimes  observed.  Black- 
smiths are  attacked  in  this  way  in  the  small  muscles  of  the  hand  ; 
drummers  in  the  extensor  and  flexor  longus  of  the  thumb  ;  dairymen 
suffer  a  paralysis  of  the  ulnar  nerve,  etc.  Other  forms  of  paralysis  and 
spasms,  as  a  rule,  require  no  treatment  in  mild  cases,  although  elec- 
tricity and  massage  may  be  employed. 

In  the  severe  forms  treatment  is  usually  of  very  little 
value.  Removal  of  the  cause,  gymnastic  exercises,  mas- 
sage, baths,  cutaneous  irritation,  actual  cautery  for  spasms. 
(For  psychic  treatment  see  under  Hysteria  and  Neuras- 
thenia.) 

2.  Diseases  of  the  Sensory  Nerves. — The  same 
causes  acting  on  sensory  nerves  produce  either  anesthesia 
in  the  area  of  distribution,  representing  the  paralytic 
symptom,  or  violent  radiating  pains,  representing  the  irri- 
tative symptom.  The  latter  are  more  important  than  the 
former.  These  neuralgic  pains,  which  occur  in  paroxysms, 
are  not  infrequently  accompanied  by  paresthesia  and  by 
some  disturbance  of  the  sensibility  in  the  affected  portion 
of  the  skin.  They  develop  most  frequently  after  severe 
infectious  diseases  (malaria,  influenza),  or  in  other  toxic 
diseases,  such  as  diabetes,  syphilis,  gout,  nephritis ;  in 
arteriosclerosis  (sciatic  nerve) ;  as  a  result  of  mechanical 
injury  (tumors,  scars,  neuromata).  Acute  spontaneous 
forms  (neuritis  ?)  may  be  accompanied  by  cutaneous  affec- 
tions, such  as  herpes  zoster,  urticaria,  and  erythema. 

For  the  diagnosis  of  neuralgia  it  is  necessary  that  the 
pain  should  correspond  exactly  to  the  area  of  distribution 


190  SPECIAL  PATHOLOGY  AND  TREATMENT. 

of  the  affected  nerve  or  nerve-trunk,  and  that  the  nerve 
should  be  sensitive  to  pressure,  especially  at  its  point  of 
exit  from  the  bony  canal.  A  neuralgic  attack  can  often 
be  provoked  by  pressure  on  these  so-called  painful  points 
(points  douloureux).  The  most  important  forms  of  neu- 
ralgia are  : 

Trifacial  Neuralgia  (Tic  Douloureux  ;  Reflex  Facial 
Spasm). — It  is  usually  confined  to  one  division  of  the 
nerve  (supra-orbital,  infra-orbital,  infra  maxillary)  and 
sometimes  to  neuralgia  of  the  tongue.  Painful  points 
correspond  to  the  exit  of  the  nerves  from  the  cranium 
(supra-orbital  notch,  infra-orbital,  and  mental  foramina). 

Occipital  Neuralgia  (Occipitalis  Major);  Intercostal 
Neuralgia  (Intercostal  Nerves);  Sciatic  Neuralgia  or 
Sciatica  (Sciatic  Nerve). — In  the  last-mentioned  form, 
which  is  extremely  refractory  to  treatment,  the  pains  radi- 
ate from  the  hip  to  the  knee,  and  in  some  cases  to  the 
outer  border  of  the  foot  (regions  supplied  by  the  sciatic 
nerve).  Painful  points  are  found  at  the  sciatic  foramina, 
in  the  middle  line  of  the  posterior  surface  of  the  thigh,  in 
the  gluteal  fold,  and  in  the  popliteal  space.  The  pain  is 
aggravated  by  flexing  the  thigh  on  the  abdomen,  with  the 
leg  extended,  owing  to  the  stretching  of  the  nerve.  The 
muscles  of  the  thigh  sometimes  atrophy,  and  curvature  of 
the  spine  may  result  (scoliosis). 

Diagnosis. — Carcinoma  of  the  rectum,  coxalgia,  and 
tabes  dorsalis  must  be  excluded.  It  is  of  the  greatest 
importance  to  examine  the  urine  for  sugar  and  albumin. 
Other  forms  of  neuralgia  are  spermatic  neuralgia,  irritable 
testes,  coccygodynia,  and  joint  neuralgias. 

Treatment. — Removal  of  the  primary  diseases  (syph- 
ilis !)  ;  galvanic  current,  using  a  low  current  strength  ; 
counterirritation  (mustard-plaster  blisters,  cupping) ;  sweat 
cures,  hot  baths,  hot  compresses  (often  better  than  ice), 
friction,  and  massage.  Antineuralgic  drugs,  such  as  sali- 
cylic acid,  anti pyrin,  analgen,  etc.  Arsenic,  potassium 
iodid.     In   severe   cases  the  use  of  morphin  and  cocain 


MULTIPLE  NEURITIS.  191 

may    be  justifiable.     Operative :  resection  of  the   nerve 
and,  in  sciatica,  stretching. 

B.  MULTIPLE  NEURITIS. 

Multiple  neuritis  or  simultaneous  disease  of  several 
nerves  is  almost  exclusively  due  to  toxic  or  infectious 
causes.  It  occurs  as  a  sequel  to  diphtheria,  tuberculosis, 
typhoid,  influenza,  and  erysipelas  ;  during  the  puerperium 
and  pregnancy  ;  in  syphilis,  gonorrhea,  diabetes,  alcohol- 
ism, and  lead  and  arsenic  poisoning,  etc. 

Anatomically  we  find  a  parenchymatous  degeneration 
(primary  disintegration  of  the  medullated  nerve-fibers), 
with  interstitial  clianges,  probably  secondary  in  character 
(round-celled  infiltration,  sclerosis).  This  is  the  so-called 
parenchymatous  neuritis  and  is  the  most  common  form,  but 
there  is  also  one  which  begins  as  a  perineuritis  and  inter- 
stitial neuritis.  It  is  probable  that  in  most  cases  the  gan- 
glion cells  in  the  anterior  horn  are  also  aifected,  although 
it  can  not  always  be  demonstrated,  but  whether  this  is 
primary  or  secondary  is  still  an  open  question. 

Course. — The  onset  of  multiple  neuritis  is  usually  acute, 
with  general  febrile  symptoms,  pain,  and  paresthesia. 
This  is  soon  followed  by  muscular  paralysis,  which  in 
severe  cases  is  later  accompanied  by  degenerative  atrophy, 
exhibiting  in  most  cases  a  definite  symmetric  distribution. 
In  other  cases  ataxic  symptoms  are  more  prominent,  com- 
bined with  nmscular  paresis.  The  muscles  most  frequently 
affected  are  the  extensors  of  the  arms  and  legs  (extensores 
digitorum  et  carpi,  quadriceps),  the  psoas,  the  peronei ; 
any  muscle  may,  however,  be  affected. 

The  reflexes  in  the  affected  region  are  abolished  ;  in 
mild  cases  they  may  also  be  increased.  Disturbances  of 
sensation  are  present  (hyperesthesia,  paresthesia,  anesthe- 
sia), and  the  muscles  may  present  the  various  reactions  of 
degeneration.  (See  Part  IV,  p.  108.)  Both  the  nerve- 
trunks  and  the  muscles  are  exquisitely  painful  on  pressure. 

After  a  variable  interval  (weeks  to  months — acute,  sub- 


192  SPECIAL  PATHOLOGY  AND  TREATMENT. 

acute,  and  chronic  forms,  see  Electric  Diagnosis)  improve- 
ment gradually  begins  and  in  most  cases  goes  on  to  com- 
plete cure.  Severe  cases  may  terminate  fatally  in  a  very 
short  time  when  the  pneumogastric  or  phrenic  nerves  are 
involved. 

We  distinguish  a  motor,  a  sensory,  and  an  ataxic  form, 
according  as  the  motor,  sensory,  or  coordinating  disturb- 
ances are  more  prominent.  It  is  difficult,  however,  to 
draw  a  sharp  dividing-line,  as  some  of  the  symptoms  of 
all  three  forms  are  usually  present.  The  ataxic  form,  on 
account  of  its  resemblance  to  tabes,  is  called  j)seudotabes. 
The  most  important  forms  are  : 

(a)  Alcoholic  Neuritis. — Motor  Form. — Flaccid  bilat- 
eral paralysis  of  the  peronei,  quadriceps,  glutei,  extensores 
carpi  et  digitorum  communis,  extensores  pollicis,  etc. 

Knee-jerks  abolished  ;  sensory  disturbances  ;  paresthe- 
sia. In  other  cases  the  radiating  pains,  paresthesia,  and 
tenderness  of  the  affected  nerves  and  muscles  are  more 
prominent ;  while  in  a  third  group  the  ataxic  gait,  muscular 
paralyses,  or  atrophies,  with  preservation  of  the  pupillary 
reflex  (in  contradistinction  to  tabes),  form  the  principal 
features  (diabetic  polyneuritis  is  a  similar  form).  At  the 
same  time  other  phenomena  of  alcoholism,  such  as  psychic 
disturbances,  delirium,  maniacal  conditions,  and  mental 
confusion  may  be  present. 

(b)  Diphtheric  Neuritis. — This  affects  chiefly  the 
motor  nerves.  Dysphagia  (spinal  accessory  and  vagus) 
and  ocular  palsies  (diplopia  and  loss  of  accommodation) 
are  the  commonest  manifestations.  In  severe  cases  the 
knee-jerk  is  abolished  and  a  flaccid  paralysis  of  the  ex- 
tremities develops.     The  vagus  may  be  paralyzed. 

(c)  Saturnine  Neuritis. — This  occurs  in  compositors, 
dyers,  etc.  The  muscles  most  commonly  affected  are  the 
extensors  of  the  hand  and  fingers  supplied  by  the  radial 
nerve  (except  the  supinator  longus).  In  addition  there 
are  sensory  irritative  phenomena :  lead  colic,  paresthesia, 
slight  disturbances  of  sensation. 


MULTIPLE  NEURITIS.  193 

(d)  Arsenical  Neuritis. — This  is  characterized  espe- 
cially by  severe  sensory  phenomena :  paresthesia  in  the 
fingers,  pain,  disturbances  of  sensibility.  Paralytic  symp- 
toms are  also  present.     (Compare  Mercurial  Neuritis.) 

Note. — Acroparesthesia  (painful  paresthesia  in  the  tips  of  the  fingers) 
without  motor  disturbances  is  a  disease  that  more  or  less  closely  re- 
sembles arsenical  neuritis.     Its  true  nature  is  unknown. 

(e)  Multiple  Neuritis  of  Pregnancy  and  the  Puer- 
perium. — The  thenar,  median,  sciatic,  and  crural  nerves 
are  specially  liable  to  be  aifected.  An  entire  extremity 
may  be  involved.  The  symptoms  are  chiefly  motor  ;  the 
reflexes  are  abolished. 

(f )  Infectious  Multiple  Neuritis. — Its  origin  is  un- 
known, but  is  almost  certainly  infectious.  It  begins  with 
general  febrile  symptoms  and  with  violent  neuralgic  pain, 
both  spontaneous  and  elicited  by  pressure  ;  muscular  weak- 
ness rapidly  develops  and  goes  on  to  a  flaccid  paralysis 
affecting  first  the  legs  and  then  the  arms  (ascending  form). 
The  tendon  reflexes  are  abolished  ;  disturbances  of  sensa- 
tion, edema,  acceleration  of  the  pulse,  and  dyspnea  (impli- 
cation of  the  vagus)  make  their  appearance.  The  duration 
is  variable  ;  most  cases  recov^er.  Death  is  due  to  paralysis 
of  the  pn'eumogastric. 

This  form  was  formerly  known  as  ^^  Landry's  paralysis.'' 
Alterations  in  the  spinal  cord,  probably  secondary  in 
character,  may  be  present  in  the  form  of  certain  definite 
degenerations.  Cases  also  occur  in  which  there  is  a  focal 
myelitis  (myeloneuritis).  A  positive  diagnosis  is  difficult. 
The  prognosis  is  unfavorable. 

Note. — A  similar  clinical  picture  is  observed  in  acute  polymyosUis, 
which  is  no  doubt  etiologically  related  to  infectious  polyneuritis.  It 
differs  from  the  latter  in  the  more  pronounced  tenderness  in  the  muscles 
on  pressure  and  the  comparative  mildness  of  the  neuritic  pains.  Sen- 
sory disturbances  and  the  reactions  of  degeneration  are  absent.  On  the 
other  hand,  there  are  febrile  constitutional  symptoms,  marked  paralytic 
conditions,  edema,  and  cutaneous  eruptions  (trichinosis  must  be  ex- 
cluded). 

Anatomically  we  find  inflammatory  alterations  in  the  muscles 
13 


194  SPECIAL  PATHOLOGY  AND  TREATMENT. 

(round-celled  infiltrations,  etc. ).     Myositic  changes  are  also  quite  fre- 
quently found  in  primary  neuritis. 

In  the  diagnosis  of  the  various  forms  of  neuritis  we 
must  exclude  the  following  conditions :  Tabes  dorsalis 
(pupillary  rigidity,  bladder  disturbances,  paralysis  of  the 
eye  muscles,  prominence  of  the  ataxic  symptoms,  compar- 
ative insignificance  of  the  muscular  paresis  in  the  initial 
stage,  history) ;  lumbar  myelitis  (bladder  disturbances,  the 
nerves  are  not  painful  on  pressure);  anterior  poliomyelitis 
(absence  of  sensory  disturbances,  of  tenderness  on  pres- 
sure, and  of  spontaneous  pains).  The  examination  of  the 
urine  for  albumin,  sugar,  and  lead  is  very  important. 

Treatment.  —  Removal  of  the  cause — alcohol,  lead  ; 
antisyphilitic,  if  indicated.  Rest,  salicylates,  antipyrin. 
Later,  electricity,  gymnastic  exercises,  massage,  and  baths. 


V.  OTHER  DISEASES  OF  THE  NERVOUS  SYSTEM 
THE  NATURE  AND  SEAT  OF  WHICH  ARE 
NOT  KNOWN. 

I.  Basedow's  disease  is  the  term  applied  to  a  group 
of  symptoms  consisting  of  exophthalmos,  struma  (vascu- 
lar), tachycardia, — paroxysmal,  pulse  100  to  160, — associ- 
ated with  other  nervous  phenomena.  The  latter  include 
tremor  of  the  extremities,  hyperidrosis,  feeling  of  heat, 
attacks  of  vomiting,  and  irritability.  The  eyeballs  are 
prominent,  and  winking  occurs  only  at  long  intervals 
(Stellwag's  sign).  There  is  lagging  of  the  upper  lid  when 
the  eyeball  is  rotated  downward  (Graefe's  sign)  and  the  in- 
ternal recti  are  often  insufficient  (Moebius'  symptom).  The 
disease  is  supposed  by  some  to  be  due  to  a  morbid  activity 
of  the  thyroid  gland  (toxic)  ;  according  to  others  the  seat 
of  the  lesion  is  in  the  medulla  oblongata. 

The  symptoms  may  be  more  or  less  pronounced  ;  in 
some  cases  they  are  barely  perceptible  (atypical  forms). 
The  disease  lasts  many  years. 

Treatment. — Bromids,  arsenic,  phosphate  of  sodium  (J 


MYXEDEMA— ACROMEGALY— TETANY.  195 

to  3  drams  per  diem).     Digitalis  has   no   effect.     Good 
food,  electricity,  friction  and  massage,  baths. 

2.  Myxedema. — As  the  development  of  myxedema  is 
accompanied  by  atrophy  of  the  thyroid  gland,  there 
appears  to  be  no  doubt  that  the  disease  has  some  connec- 
tion with  this  structure.  The  immediate  cause  appears  to 
be  the  absence  of  its  secretion  (the  opposite  condition  to 
that  which  obtains  in  Basedow's  disease  ?).  Total  extir- 
pation of  the  thyroid  gland  is  followed  by  a  similar  con- 
dition (cachexia  strumipriva). 

The  chief  symptom  of  myxedema  consists  in  a  dis- 
figuring edema  in  the  skin  of  the  face  and  hands.  The 
skin  becomes  thick  and  diy,  and  its  upper  layers  desqua- 
mate. The  movements  are  clumsy  and  uncertain.  The 
mental  condition  is  affected  :  the  subject  becomes  apathetic 
and  finally  demented. 

Treatment. — Good  results  are  obtained  by  the  adminis- 
tration of  thyroid  gland  in  substance,  by  subcutaneous 
injection  of  the  juice,  and  by  the  use  of  glycerin  extract, 
thyroid  gland  tablets,  and  thyreoidinum  siccum  internally. 

3.  Acromegaly. — In  this  mysterious  disease  there  is 
slow,  abnormal  growth  of  the  fingers,  hands,  feet,  nose, 
lips,  and  jaws  (the  "  points,'^  "  akra,''  of  the  body),  lead- 
ing to  permanent  disfigurement.  Optic-nerve  atrophy  and 
ocular  palsies  frequently  result  from  the  pressure  of  the 
enlarged  pituitary  body  in  the  sella  turcica.  Glycosuria 
is  often  present. 

Other  processes  belonging  under  this  head  have  been 
discussed  in  Part  IV,  4  (hemiatrophia  facialis,  edema  cutis 
circumscriptum,  erythromelalgia,  symmetric  gangrene). 

4.  Tetany. — This  consists  in  paroxysmal  attacks  of 
painful  tonic  spasms,  affecting  especially  the  flexor  muscles 
of  the  fingers  ("Pfotchenstellung'^;  main  en  griffe),  arms, 
and  toes.  The  spasms  are  symmetric  and  can  be  pro- 
voked by  pressure  on  the  nerve-trunks  (Trousseau's  phe- 
nomenon). The  attacks  may  occur  at  intervals  for  several 
weeks  or  more. 


196  SPECIAL  PATHOLOGY  AND  TREATMENT. 

Note. — Tetanic  spasms,  especially  of  the  flexors  of  the  fingers  and 
muscles  of  the  calf,  are  frequently  seen  in  neuritis,  in  alcoholic  sub- 
jects, and  in  persons  suffering  from  gastric  disturljances.  They  may, 
however,  also  occur  in  otherwise  healthy  persons  (manual  workers, 
etc.). 

Tetanus  is  a  septic  disease  following  wounds  and 
is  caused  by  the  toxins  of  the  tetanus  bacillus.  It  is  a 
secondary  infection  which  may  occur  after  slight  injuries, 
manifesting  itself  in  tonic  convulsions  affecting  all  the 
muscles  of  the  body. 


PART  VI. 

GENERAL  REMARKS  ON  AUTOPSY  TECHNIC 

AND  THE  MICROSCOPIC  EXAMINATION 

OF  THE  NERVOUS  SYSTEM. 

In  opening  the  cavity  of  the  skull  and  spinal  column 
it  must  always  be  borne  in  mind  that  a  microscopic 
examination  of  the  central  organs  may  eventually  be 
necessary.  In  many  cases  the  exact  anatomic  condition 
can  not  be  determined  without  this  examination,  as 
the  macroscopic  appearances,  while  they  may  explain  a 
coarse  focal  lesion,  do  not  suffice  to  determine  which  of  the 
diiferent  forms  of  degenerative  disease  is  present.  This 
cardinal  rule  is  often  violated. 

The  autopsy  in  such  cases  should  be  performed  as  soon 
after  death  as  possible,  never  later  than  twenty-four  hours. 
In  diseases  of  the  spinal  cord  the  body  should  be  laid  on 
its  face,  to  avoid  the  confusing  eifects  of  postmortem 
gravitation. 

The  greatest  mistake  made  in  autopsies  which  may  in 
other  respects  be  correctly  performed  consists  in  carelessly 
cutting,  compressing,  and  distorting  the  brain  and  cord, 
often  rendering  it  impossible  subsequently  to  make  a 
proper  microscopic  examination. 

The  first  point  is  the  removal  of  the  brain.  If  the 
membranes  (tentorium,  etc.)  are  not  completely  loosened 
and  the  cervical  cord  and  cranial  nerves  carefully  divided, 
the  brain  can  not  be  removed  without  an  undue  amount 
of  pulling,  which  may  destroy  parts  of  the  brain  that 
have  undergone  softening.  In  the  next  place  an  un- 
necessary number  of  incisions  are  too  often  made  in  the 
central  ganglia,  the  corpora  quadrigemina,  etc.,  so  that  it 
is  very  difficult  later  to  recognize  the  parts  in  serial  sections. 

197 


198  AUTOPSY  TECHNia 

It  is  customary  to  make  these  incisions  obliquely  through 
the  central  ganglia,  thus  disturbing  the  relations  of  the  soft 
tissue  of  the  brain  to  such  an  extent  that  it  is  impossible 
afterward  to  orient  one's  self  in  a  microscopic  section. 
The  incisions  in  such  cases  should  always  be  made  exactly 
horizontal  or  exactly  frontal ;  it  is  best  to  avoid  cutting 
the  fresh  brain  altogether. 

The  brain  must  never  come  in  contact  with  water,  as 
this  gives  rise  to  misleading  appearances  when  the  brain 
is  hardened. 

After  opening  a  diseased  focus  by  a  superficial  hori- 
zontal cut,  it  is  much  better  not  to  attempt  any  fresh  inves- 
tigation of  the  details.  It  is  not  likely  that  any  more  will 
be  learned,  no  matter  how  many  incisions  are  made.  The 
minute  examination  should  be  deferred  until  the  brain  has 
been  hardened  in  formalin  (aqueous  solution,  20  to  30^) 
from  six  to  eight  days  and  then  in  Miiller's  fluid. ^  If 
the  brain  is  kept  at  a  temperature  of  30°  C,  and  if  the 
lateral  ventricles  are  opened  and  the  corpus  callosum  de- 
tached, the  examination  can  be  made  after  a  few  weeks 
without  doing  any  damage.  It  will  then  be  much  easier 
to  recognize  the  relations  of  the  parts,  and  degenerations 
which  could  not  be  seen  in  the  recent  condition  are  re- 
cognized at  the  first  glance. 

The  spinal  cord  is  often  injured  by  careless  use  of  the 
chisel  and  forceps ;  mere  tugging  and  squeezing  may 
lacerate  a  softened  area.  In  the  case  of  the  cord  also  the 
caution  against  making  too  many  incisions  should  be 
remembered.  In  dividing  the  posterior  roots  it  is  well  to 
cut  as  far  out  as  possible,  so  as  to  obtain  a  part,  at  least, 
of  the  spinal  ganglia  along  with  the  posterior  roots.  This 
is  always  possible  in  the  lumbar  enlargement. 

After  carefully  considering  the  course  of  the  disease, 
the  examiner  should  make  up  his  mind  before  the  autopsy 
what  nerves  or  muscles  are  probably  diseased  and  ought 

^  Bichromate  of  potassium  2  gm.,  sulphate  of  sodium  1  gm.,  distilled 
water  100  cc. 


AUTOPSY  TECHNIC.  199 

to  be  taken  out.  The  nerves  are  secured  to  small  pieces 
of  wood,  and,  like  the  muscles,  carefully  labeled  with 
the  name,  side  of  the  body,  and  level  at  which  they 
were  removed.  The  report  of  the  autopsy  should  be  as 
minute  as  possible.  The  condition  of  the  bones  of  the 
skull  and  spinal  column  and  of  the  meninges  and  blood- 
vessels should  be  accurately  described  and  the  contents  of 
the  ventricles  noted.  The  latter  point  should  be  determined 
before  the  brain  is  removed  ;  all  measurements  must  be 
made  on  the  fresh  preparation. 

In  some  cases,  especially  in  recent  focal  diseases,  the 
microscopic  examination  can  be  made  at  once  without 
hardening  the  tissue.  A  small  piece  is  excised  with  the 
scissors,  placed  on  a  slide,  and  teased.  In  this  way 
granule  cells,  degenerated  nerve-cells  and  fibers,  and 
degenerated  muscle-fibers  can  be  recognized.  To  bring 
the  parts  out  more  clearly  the  slide  may  be  rapidly  stained 
with  a  drop  of  1  per  cent,  methylene-blue  solution  or  with 
hematoxylin. 

Degenerated  portions  of  tissue  are  cut  into  small  pieces 
and  immediately  placed  in  a  1  per  cent,  solution  of  osmic 
acid,  which  is  to  be  kept  in  the  dark.  After  twenty-four 
hours  the  products  of  degeneration  (fat  granules)  will  be 
stained  black.  This  proceeding  (Marchi's  method)  is  even 
more  successful  in  tissue  hardened  in  Miiller's  fluid  (not 
in  alcohol). 

Whenever  it  is  desired  to  make  a  systematic  examina- 
tion, hapdening  is  absolutely  indispensable.  The  best  re- 
sults are  obtained  with  Miiller's  fluid  or  alcohol,  depend- 
ing on  the  particular  tissue  it  is  desired  to  examine.  For 
the  examination  of  nerve-fiber  (degenerations)  Miiller^s 
fluid  must  be  used  ;  if  the  condition  of  the  ganglion  cells 
(inflammatory  degenerative  processes)  is  to  be  investigated, 
the  tissue  must  be  hardened  in  alcohol.  In  other  cases 
the  tissue  may  be  first  hardened  in  formalin. 

It  is  often  desired  to  examine  both  fibers  and  ganglion 
cells.     In  such  a  case  the  cells  can  be  fairly  well  stained 


200  AUTOPSY  TECHNIC. 

when  the  tissue  is  hardened  in  Miiller's  fluid.  It  is  much 
better,  on  the  whole,  to  put  the  greater  part  of  the  brain, 
spinal  cord,  nerves,  and  muscles  into  Midler's  fluid  after 
it  has  been  hardened  in  formalin,  and  to  harden  some 
of  the  more  important  smaller  pieces  in  absolute  alcohol 
immediately  after  removal  from  the  body.  Such  prepara- 
tions can  also  be  stained  for  bacteria. 

It  requires  several  months  to  harden  a  brain  in  Miiller's 
fluid.  The  time  can,  however,  be  considerably  shortened 
by  keeping  the  jar  in  a  temperature  of  about  30°  C. 

The  solution  must  be  constantly  renewed  ;  during  the 
first  six  days,  if  the  jar  is  kept  in  a  warm  place,  the  solu- 
tion should  be  renewed  every  day,  later  at  longer  intervals. 
As  the  hardening  process  goes  on  additional  incisions, 
either  horizontal  or  frontal,  should  be  made  from  time  to 
time  to  allow  the  chrome  salts  to  penetrate  the  tissue  more 
easily.  The  tissues  should  never  be  examined  until  they 
are  completely  hardened ;  the  pieces  must  be  brown,  not 
yellow.  If  the  hardening  is  incomplete,  impleasant  arti- 
facts will  be  produced  when  the  tissue  is  stained. 

Hardening  in  absolute  alcohol  requires  only  a  few  days. 
The  alcohol  should  be  changed  several  times.  After  a 
tissue  has  been  hardened  in  Miiller's  fluid  it  is  to  be  cut 
in  thin  slices  and  hardened  again  in  alcohol,  but  without 
dehydrating,  if  it  is  intended  to  use  a  medullary  sheath 
stain.  The  tissue  is  then  placed  first  in  thin  and  then 
in  thick  celloidin  for  the  purpose  of  imbedding.  After 
an  interval  varying  from  five  to  twenty  days,  ^or  even 
longer,  depending  on  the  size  of  the  pieces,  the  tissues  are 
mounted  on  blocks  and  laid  in  70  per  cent,  alcohol ;  after 
a  few  hours  they  are  ready  to  cut. 

The  cutting  is  done  with  a  microtome,  and  the  sections 
need  not  be  very  thin.  If  an  uninterrupted  series  of 
sections  is  desired,  a  piece  of  firm  medicated  toilet-paper, 
which  has  been  previously  labeled,  is  moistened  with  a 
sugar  solution,  placed  on  a  plate,  and  covered  with  a  layer 
of  thin  celloidin.     The  sections  are  then  laid  in  order  on 


AUTOPSY  TECHNia  201 

the  paper,  to  which  they  immediately  adhere.  This  is 
kept  ill  70  per  cent,  alcohol.  When  the  sections  are  to  be 
examined,  they  are  easily  loosened  from  the  paper  by 
placing  the  latter  in  water.  To  stain  the  nerve-fiber, 
Weigert-PaPs  hematoxylin  stain  for  medullary  sheaths  is 
used.  To  stain  the  cells  carmin  or  double  carmin  stain  is 
used  for  tissues  hardened  in  Miiller's  fluid,  and  NissFs 
methylene-blue  for  tissues  hardened  in  alcohol.  (For 
further  directions  the  student  is  referred  to  the  text- 
books of  Kahldon,  Friedliinder-Eberth,  and  others.) 

With  the  medullary  sheath  stain  all  the  medullated 
nerve-fibers  are  stained  black ;  hence  if  such  fibers  are 
normally  absent,  or  if  they  are  degenerated  or  destroyed, 
the  corresponding  areas  are  not  stained  and  appear  pale 
instead  of  black.  The  fatty  constituents  of  the  medullary 
sheath  enter  into  a  firm  chemic  union  with  the  pigment  of 
the  hematoxylin,  and  this  produces  the  black  color. 

The  most  modern  method,  Golgi's  impregnation  with 
silver  (Cajal),  can  be  used  in  pathologic  cases  only  under 
certain  restrictions,  as  it  does  not  work  uniformly  well. 

Our  knowledge  of  the  structure  of  the  nervous  system 
has  been  gained  chiefly  by  means  of  the  following  methods 
of  investigation  : 

1 .  By  reconstruction  of  serial  sections  through  a  normal, 
fully  developed  human  brain  (Stilling,  Meynert,  etc.), 
various  methods  of  staining  or  impregnation  being  used 
(Weigert,  Golgi,  Cajal,  and  Nissl). 

2.  By  the  examination  of  pathologic  cases,  especially  of 
secondary  degenerations  (Tiirck,  Waller). 

3.  By  comparative  anatomy  and  comparative  embryol- 
ogy (Meynert,  Edinger,  and  others). 

4.  By  a  study  of  the  development  (medullation,  etc. 
Kolliker,  Kupffer,  His,  Flechsig,  and  others). 

5.  By  the  examination  of  degenerations  produced  ex- 
perimentally (Gudden,  Monakow,  and  others). 

These  methods  have  been  used  as  much  as  possible  in 
the  preparation  of  the  plates  contained  in  this  atlas. 


BIBLIOGRAPHY. 


The  following  works,  which  have  been  utilized  by  the  author  in 
the  preparation  of  this  epitome,  are  recommended  as  admirable  refer- 
ence books  for  students  of  neurology: 


1.  Anatomy. 

The  text-books  of  Koelliker  (Gewebelehre),  Henle,  HofEmann- 
Schalbe,  Raube,  Gegenbaur.  Monographs:  von  Flechsig  (Leitungs- 
bahnen,  Plan  des  menschlichen  Gehirns),  Lenhossek  (minute  struc- 
ture), Edinger  (twelve  lectures),  v.  Gehuchten  (Gehirnanatomie), 
Bechterew  (Leitungsbahnen),  Obersteiner  (Anleitung  zum  Studium 
der  nervosen  Organe).  The  works  of  Meynert,  Gudden,  His,  Golgi, 
Caval,  and  others. 


2.  Physiology  and  Pathology. 

Charcot  (lectures),  Erb  (Electrotherapie,  Riickenmarkskrankheiten 
in  "Ziemssen's  Handbuch,"  vol.  xi),  v.  Striimpell  (text-book), 
Leyden  (clinical  lectures),  Wernicke  (Gehirnkrankheiten),  Gowers 
("Diseases  of  the  Nervous  System"),  Seeligmiiller  (text-book),  P. 
Marie  (lectures),  Liebermeister  (lectures),  Eulenburg  (article  on 
"Nervous  Diseases"  in  the  Encyclopedia),  Mendel  (ibid.,  article  on 
the  "Brain"),  Oppenheim  (text-book),  Hirt  (text-book),  Dejerine 
("Centres  Nerveux").  Leube  (diagnosis);  the  works  of  Westphal, 
Kussmaul,  Nothnagel,  Munk,  Hitzig,  Lichtheira,  Ferrier,  and  many 
others. 


202 


ABBREVIATIONS  USED  IN 
FIGURES. 


THE 


a.  .   . 

.  Anterior. 

c.  1.  a. 

.  Anterior  limb  of  inter- 

A. b. 

.  Basilar  artery. 

nal  capsule. 

A.  c  c. 

.  Artery  of  corpus  callosum 

c.  1.  p. 

.  Posterior  limb  of  inter- 

(commissural artery). 

nal  capsule. 

a.  1.    . 

.  Ansa  lentiformis. 

c.L.  . 

.  Luys'  body,  subthalamic 

a.  d.  . 

.  Descending  root  of  audi- 

body. 

tory  nerve. 

CI.     . 

.  Column  of  Clarke. 

A.  S. 

.  Aqueduct  of  Sylvius. 

CI.     . 

.  Claustrum  (brain). 

A.  f.  s. 

.  Sylvian    artery,    middle 

c.  m. 

.  Middle  commissure. 

cerebral  artery. 

C.  p. 

.  Posterior  horn  of  spinal 

A.  V. 

.  Vertebral  artery. 

cord. 

a.  V.  . 

.  Arch  of  vertebra. 

c.  p.  . 

.  Posterior  horn  of  lateral 

B.  .    . 

.  Brachium    (superior  pe- 

ventricle. 

duncle  of  cerebellum). 

c.  p.  . 

,  Posterior  commissure. 

Bulb.olf.  Olfactory  bulb. 

c.  q.  a. 

.  Anterior  corpus  quadri- 

c.    .   . 

.  Conarium,  pineal  body. 

geminum. 

C.   a. 

.  Anterior  horn  of  spinal 

c.  q.  p. 

.  Posterior  cor})us  quadri- 

cord. 

geminum. 

c.  a.  . 

.  Anterior  commissure 

c.  r.  . 

.  Restiform  body. 

(brain  and  cord). 

c.  sbth. 

Subthalamic  body. 

c.  a.  . 

.  Anterior  horn  of  lateral 

C.    St. 

.  Corpus  striatum. 

ventricle. 

c.  t.    . 

.  Central  tegmental  tract 

c.  Am. 

.  Cornu  Ammonis, 

(fillet). 

Cb.    . 

.  Cerebellum    and    direct 

c.   tr. 

.  Corpus  trapezoides. 

cerebellar  tract  in  cord 

cun.  . 

.  Cuneus. 

and  medulla. 

C.  V. 

.  Centrum    semiovale    of 

c.  c.  . 

.  Corpus  callosum. 

Vieussens. 

c.  c.  . 

.  Corpus  candicans  or  albi- 

d.  .    . 

.  Dura  mater. 

cans. 

D.  Br. 

.  Decussation  of  brachia. 

c.  e.  . 

.  External  capsule. 

Dec.  Py 

r.  Decussation     of     pyra- 

cerv. 

.  Cervical. 

mids. 

c.  g.  1. 

.  External    geniculate 

Ea.  R. 

.  Reactions    of    degenera- 

body. 

tion. 

c.  g.  m. 

Internal      geniculate 

f.    .    . 

.  Foi-nix. 

body. 

f.  a.   . 

.  Anterior  ground  bundle. 

Ch.     . 

.  Optic  chiasm. 

f.  a.  e. 

.  External  arciform  fibers. 

C.  i.  . 

.  Internal  carotid. 

f.  a.  i. 

.  Internal  arciform  fibers. 

203 


204 


ABBREVIATIONS  USED  IN  THE  FIGURES. 


f.  al. 

.  Auterolateral    ground 

n.  VIII 

bundle  (mixed  lateral 

d.     . 

.  Dorsal  nucleus  of  audi- 

zone). 

tory  nerve. 

f.  B.  . 

.  Funiculus  cuneatus. 

n.VIII^ 

-.  Ventral  nucleus  of  audi- 

f. c.   . 

.  Calcarine  fissure. 

tor}'  nerve. 

f.  d.  . 

.  Descending  fornix. 

n.  v.  . 

.  Red  nucleus. 

f.  G.  . 

.  Funiculus  gracilis. 

O.  .    . 

.  Olive  (inferior,  greater). 

Fl.     . 

.  Flocculus. 

ol.  m. 

.  Mesial  accessory  olive. 

fl.  .    . 

.  Lateral  gi'ound  bundle. 

ol.  p. 

,  Posterior  accessory  olive. 

f.  1.    . 

\  Posterior      longitudinal 
/     bundle. 

ol.  s. 

.  Superior  olive. 

f.  1.  p. 

p.  .    . 

.  Pia. 

f.p.   . 

.  Posterior  column. 

p.  .    . 

.  Posterior. 

F.  rhomb.  Rhomboid  fossa. 

Ped.  . 

.  Cerebral  peduncle,  pes. 

f.  S.  . 

.  Fissure  of  Sylvius. 

crusta  pedunculi. 

G.      . 

.  Gowers'  tract. 

PI.  ch. 

.  Choroid  plexus. . 

g.  ang 

Angular  gyrus. 

Pulv. 

.  Pulvinar. 

g.  cent 

Central  convolutions. 

Put.  . 

.  Putamen. 

g.  fr. 

.  Frontal  convolution. 

Py-   • 

.  Pj^ramidal  tract. 

g.H. 

Hippocarapal     convolu- 

q. a.  . 

.  Anterior  corpus  quadri- 

tion. 

geminum. 

gl-  P- 

Globus  pallidus  (middle 

q.  p.  . 

.  Posterior  corpus  quadri- 

and  inner  zones  of  len- 

geminum. 

ticular  nucleus). 

R.      . 

.  Raphe  of  the  tegmentum 

g.l.   . 

.  External    geniculate 

and  pons. 

body. 

r.  a.  . 

.  Anterior  root. 

g.  m. 

.  Internal     geniculate 

R.  c. 

.  Ramus  arteriosus    com- 

body. 

municans. 

g.  0.    . 

.  Occipital  convolution. 

r.  p.  . 

.  Posterior  root. 

G.  0. 

.  Gratiolet's  optic    radia- 

R. subth.  Subthalamic  region. 

tion. 

S.  a.  . 

.  Anterior   longitudinal 

g.  sm. 

.  Supramarginal  gyrus. 

sulcus. 

g.t.   . 

.  Temporal        convolu- 

S. .    . 

.  Solitary    bundle    (de- 

tion. 

scending  root    of    IX 

K.      . 

.  Raph6    of    the  tegmen- 

and X). 

tum. 

s.g. . 

.  Substantia  gelatinosa, 

L.  .    . 

.  Boundary   zone  of   Lis- 

posterior  horn. 

sauer. 

S.n.  . 

.  Substantia  nigra. 

L.  .    . 

.  Lenticular  nucleus. 

S.p.  . 

Posterior      longitudinal 

L.  .    . 

.  Lateral. 

sulcus. 

l.pc. 

.  Paracentral  lobule. 

s.  p.  . 

.  Septum  lucidum. 

m. 

.  Mesial. 

S.  r.  t. 

Substantia  reticularis  of 

M.  ob. 

.  Medulla  oblongata. 

tegmentum. 

n.   .    . 

.  Nodulus. 

str.      s. 

N.am. 

.  Amygdaloid  nucleus. 

m.,  i. 

Superior,    middle,    and 

N.  B. 

.Nucleus  of   Burdach, 

inferior  layer. 

cuneate  nucleus. 

St.  a. 

.  Striae  acusticae. 

n.  c.  . 

.  Caudate  nucleus. 

t.    .    . 

.  Taenia  thalami. 

n.  f.  a. 

.  Arciform  nucleus. 

T.  teg. 

.  Tegmentum. 

N.  G. 

.  Nucleus  of  GoU,  nucleus 

Th. 

.  Optic  thalamus. 

of  the  clava. 

tr.  0. 

.  Optic  tract. 

ABBREVIATIONS  USED  IN  THE  FIGURES. 


205 


trig,  olf , 

.  Trigonuni  olfactoriuui. 

V.  m.  a. 

Anterior     medullary 

U.      . 

.  Uvula    (vermiform  pro- 

velum (with  lingula). 

cess  of  cerebellum). 

z.  v.  . 

.  Root-zone. 

Tine.  . 

.  Uncus     (Hippocampal 

V.c.  . 

.  Caudal,  descending  root 

gj'nis). 

of  trigeminus. 

V.      . 

.  Ventricle     (lat.,     med., 

V.  m.    , 

.  Motor    nucleus    of    tri- 

III). 

1 

geminus. 

V.  IV. 

.  Fourth  ventricle. 

V.  n.     , 

,  Nasal    descending    root 

V.  s. 

,  Superior      vermiform 

of  trigeminus. 

process     of      cerebel- 

V. s.     . 

,  Sensory  nucleus  of   tri- 

lum. 

geminus. 

V.  i.  . 

.  Inferior   vermiform 

VIII    c. 

process     of      cerebel- 

N.   .    , 

.  Cochlear  nerve. 

lum. 

VIII   V. 

V.    .    . 

,  Vertebra. 

IN.., 

.  Vestibular  nerve. 

INDEX. 


Abducens  nerve,  18 

lesions  of,  symptoms,  99 
motor  pathway  in,  45 
Abscess,  brain,  147;  PI.  60,  Fig.  1 
Achilles  tendon  reflex,  121 
Acquired  diseases,  77 
Acromegaly,  195 
Afterbrain,  23 
Ageusia,  central,  87 
Akinesia  algera,  161 
Alcoholic  neuritis,  192 
Alexia,  125,  127 
Amnesia,  128 
Amnesial  aphasia,  125 
Amygdaloid  nucleus,  10 
Amyotrophic  lateral  sclerosis,  177; 
PI.  63,  Fig.  3 
section  of  cord  in,  PI,  78 
Analgesia,  116 
Anemia  of  brain,  141 
Aneurysm  of  brain,  146;  PI.  59, 

Fig.  1 
Anode,  109 
Anosmia,  central,  87 
Anterior  columns  of  cord,  15,  38 

commissure,  11 

poliomyelitis,  180 
Aphasia,  124 

amnesial,  125,  127 

motor,  124,  125 

optic,  125 

sensory,  86,  125 

visual,  86 
Apoplectic  stroke,  143 
Apoplexy,  PL  65 
Aqueduct  of  Sylvius,  12 
Arachnoid,  2 
Arc  de  cercle,  160 
Archineuron,  40 


Arcuatus,  30 
Arsenical  neuritis,  193 
Arteries  of  brain,  20 

of  spinal  cord,  20 
Arteriosclerosis  of  brain,  147 
Articulation,  disturbances  of,  124 
Ascending  degeneration  of  spinal 

cord,  PI.  73 
Association  fibers,  30 
Astrocytes,  25 
Ataxia,  108 

Friedreich's,  105 

hereditary,  105,  185 
Ataxic  gait,  108 

w^riting,  126 
Athetoid  movements,  107 
Atrophy,  neurotic  muscular,  PI. 
64,  Fig.  5 

spinal  muscular,  104 
Auditory  nerve,  18 

lesions  of,  symptoms,  99 
sensory  pathway  of,  61 
Autopsy  technic of  nervous  system, 

197 
Axillary  nerve,  lesions  of,  symp- 
toms, 100 
Axis-cylinder  process,  28 

Basal  forebrain  bundle,  36 
ganglia,  horizontal  section  of, 
Pi.  9 

Base  of  brain,  disease  of,  symp- 
toms, 91 

Basedow's  disease,  194 

Basilar  meningitis,  138 

Bladder,  examination  of  functions 
of,  122 
motor  pathway  of,  49 
sensory  nerves  of,  59 


207 


208 


INDEX. 


Blindness,  psychic,  86 
Blood-vessels  of  brain,  diseases  of, 

136 
Brachial  monoplegia,  85 

plexus,  Erb's  paralysis  of,  96 
Bradylalia,  124 
Brain,  anatomy  of,  1 

anemia  of,  141 

aneurysm  of,  146;  PI.  59,  Fig.  1 

arteriosclerosis  of,  147 

base  of,  PL  5 

circulatory  disturbances,  141 

development  of,  PL  16 

embolic  softening,  PL  62,  Fig.  2 

horizontal  section  of,  PL  6 

hyperemia  of,  141 

in  situ,  PL  1 

mesial  surface,  PL  4 

of   dog,   four  coronal    sections 
through,  PL  11 

outer  surface  of,  PL  3 

tumor  of,  PL  59,  Fig.  3 

ventricular  system  of,  PL  7 

vesicles,  primary,  22 

with  meninges  removed,  PL  2 
Brain-abscess,  147;  PL  60,  Fig.  1 
Brain-embolism,  145 
Brain-stem,  PL  10 

coronal  section  through,  PL  12, 
13 
Brain-substance,  diseases  of,  141 
Brain-syphilis,  139 
Brain-thrombosis,  145 
Brain-tumor,  149 
Breschet's  venous  plexus,  21 
Bulbar  paralysis,  104,  155 

speech,  124 
Burdach,  funiculus  of,  15 

Calamus  scriptorius,  15 
Calf  muscles,  spasm  of,  188 
Capsula  Reilii,  10 
Capsule,  external,  10 
Caries  of   vertebra,  PL    59,   Fig. 
2 

Cathode,  109 

Cauda  equina,  lesions  of,  symp- 
toms, 95 
Caudate  nucleus,  5 

development  of,  23 


Causes  of  diseases  of  nervous  sys- 
tem, 75 
Cella  media,  6 
Cells,  galvanic,  108 
Central  convolutions,  3 

disease  of,  symptoms,  84 
motor  neuron,  40 

symptoms  of  lesion  of,  82 
pathway,  35 
neuron,    system    disease   of, 

symptoms,  104 
neurons,  26 
nuclear  layer,  25 
sensory  neuron  complex,  51 

pathway,  33 
sulcus,  3 
Centripetal  sensory  path,  system 

disease  of,  sj^mptoms,  105 
Centrum   semiovale,  disease    of, 
symptoms,  87 
Vieussenii,  5 
Cephalalgia,  163 
Cerebellar  convolution,  PL  20 

cortex,  PL  19 
Cerebellum,  12 
development  of,  24 
influence   of,   in   coordination, 

73 
lesions  of,  symptoms,  90 
Cerebral  convolutions,  PL  20  and 
21 
hemorrhage,  142 
neuroses,  157 
paralysis,  characters  of,  91 
Cerebrospinal     meningitis,     epi- 
demic, PL  58 
sclerosis,  multiple,  PL  77 
Cervical  enlargement,  lesions  of, 

symptoms,  93 
Chiasm,    lesions    of,    svmptoms, 

97 
Chorea,  chronic  hereditary,  166 
Huntingdon's,  166 
minor,  165 
Sydenham's,  165 
Clioreic  movements,  107 
Choroid  plexuses,  9 
Cingulum,  30 
Circle  of  Willis,  20 
Claustrum,  10 


INDEX. 


209 


Clonic  spasm,  107 
Cochlear  nerve,  lesions  of,  symp- 
toms, 99 
sensory  pathway  of,  HI 
Collaterals,  :IH 
Columns  of  spinal  cord,  :>H 
Combined  system  disease,  78;  PI. 

82,  105 
Commissural  fibers.  30 
Compression  myelitis,  169;  PI.  75, 
Fig.  3 

of  spinal  cord,  169 
Conarium,  11 
Concept,  67 

Congenital  myotonia,  166 
Conjunctival  reflex,  120 

arc,  65 
Conscious  processes,  66 
Consciousness,     disturbances    of, 

128 
Contents  of  consciousneas,  68 
Contracture,  107 
Contractures,  hysteric,  160 
Convolution,  central,  3 

cerebral,  development  of,  23 

inferior  marginal,  4 
temporal,  4 

occipitotemporal,  4 

supramarginal,  4 
Convulsion,  107 
Coordination,  72 

centers,  73 

examination  of,  108 
Cord,  compression  of,  169 

diseases  of,  167 

posterior  columns  of,  15 
Cornu  ammonis,  6 
Corona  radiata,  32 
Corpora  quadrigemina,  12 

lesions  of,  symptoms,  88 
Corpus  callosum,  5 

disease  of,  symptoms,  87 

dentatum  cerebelli,  14 

striatum,  5,  8 
disease  of,  symptoms,  88 

subthalamicura,  11 
Cortex  cerebri,  3 

Cortical  lesions,  symptoms  of,  84  j 
Corticomuscular    motor     path,    ; 

symptoms  of  disease  of,  104  j 

14 


Cranial  nerves,  17 

development  of,  26 
distribution  of,  PI.  27 
lesions  of,  symptoms,  96 
Cremaster  reflex,  120 
Crural  monoplegia,  85 

nerve,  lesions  of,  symptoms,  101 
Crus  ascendens  fornicis,  7 
Crusta,  5 
secondary  degenerations  of,  PI. 
67,  68 
Cuneiform  lobe,  14 
Cuneus,  4 

Cutaneous  reflex  arc,  64 
reflexes,  119 

Decussation  of  pyramids,  15 
Degeneration  of  nerve-cells  and 
fibers,    products  of,    PI.   63, 
Fig.  a-f 

reaction  of,  110 
Deitera'  cells,  28 

nucleus,  62 
Dementia,  paralytic,  152 
Dendrites,  PI.  17 
Dendrons,  28 
Descending  degeneration  in  spinal 

cord,  PI.  72 
Development  of  nervous  system, 

22^ 
Diagnosis,  128 

electric,  108 

methods  of,  106 
Diaphragm,  spasm  of,  188 
Digitationes  cornu  ammonis,  6 
Diphtheric  neuritis,  192 
Diplegia,  85 
Dura  mater,  1 
Dysarthria,  124 
Dysgraphia,  126 
Dyslexia,  126 
Dystrophy,  progressive  muscular, 

104,  179;  PI.  64,  Fig.  4 

Eclampsia  infantum,  164 
Electric  diagnosis,  108 

treatment,  134 
Electromotive  force,  109 
Embolic  softening  of  brain,  PI.  62, 

Fig.  2 


210 


INDEX. 


Embolism,  brain,  145 
Embolus,  14 
Embryonal  area,  PI.  15 
Encephalitis,  acute  hemorrhiigic, 
PI.  61,  Fig.  2 
nonsuppurative,  148 
Endogenous  diseases,  76 
Epilepsy,  163 

Epileptiform  convulsions,  107 
Epiphysis,  11 

Erb's  paralysis  of  }>rachial  plexus, 
,  96 

Etat  de  mal,  164 
Examination,  methods  of,  106 
of  bladder  function,  122 
of  coordination,  108 
of  external  condition  of  mus- 
cles, 106 
of  memory,  127 
of  motor  irritative   symptoms, 
107 
power,  107 
sphere,  106 
of  pain  sense,  116 
of  reflexes,  119 
of  sense  of  hearing,  118 
of  smell,  118 
of  taste,  119 
of  weight,  116 
of  sensory  sphere,  118 
of  sight,  117 
of  speech,  124 
of  tactile  sense,  113 
of  temperature  sense,  116 
of  topographic  sense,  115 
of  trophic  disturbances,  123 
of  vasomotor  disturbances,  123 
of  writing  power,  127 
with  faradic  current,  111 
Exogenous  diseases,  77 
External  capsule,  10 
Extraspinal  fibers,  38 

Facial  monoplegia,  85 
nerve,  18 

lesions  of,  symptoms,  99 
motor  pathway  in,  45 
spasm  of,  188 
spasm,  reflex,  190 
Falx  cerebri,  2 


Faradic     current,      examination 

with,  111 
Fascia  dentata,  6 

tarini,  6 
Fasciculus  longitudinalis  inferior, 
30 
superior,  30 

occipitofrontalis,  30 

uncinatus,  30 
1   Fibers,  association,  30 

commissural,  30 

extraspinal,  38 

intramedullary,  38 

lateral  peduncular,  34 

mesial  peduncular,  33 

microscopic  examination  of,  199 

myelogenic,  38 

projection,  32 
Fibrise  proprite,  30 
Fibrillary  muscular  contractions, 

83 
Fifth  nerve,   motor  pathway  in, 
44 

ventricle,  8 
Fillet,  54 

atrophy  of,  PI.  70,  Fig.  3 

tract  of,  33 
Fimbria,  6 
Fissure  of  Rolando,  3 

of  Sylvius,  4 

development  of,  23 

parieto-occipital,  4 

Simian,  3 

triradiate,  5 
Fissures,    cerebral,    development 

of,  23 
Flocculus,  14 
Focal  disease,  78 

symptoms  of,  84 
Folia  cacuminis,  13 
Foot-drop,  102 
Foramen  of  Monro,  9 
Forebrain,  22 
Fornix,  pillars  of,  7 
Fourth  ventricle,  13 
Friedreich's  ataxia,  105 

disease,  185 
Frontal  lobe,  3 

diseavse  of,  symptoms,  84 

pontine  tract,  34 


INDEX. 


211 


Functional  diseases,  7H 
Funiculus  anterior,  15 

cuneatus,  15 

gracilis,  15 

Gait,  108 

Galvanic  examination  of  muscles, 

108 
Gangliated  cord  of  sympathetic, 

19 
Ganglion  habenulae,  11 

impar,  19 

intervertebral,  19 
Ganglion-cells,  27  ;  PI.  18 

development  of,  26 
Ganglionic  cord,  22 
Genu  of  corpus  callosum,  5 
Girdle  pains,  170 
Glia  cells,  25;  PI.  18 
Globus  pallidus,  10 
Glossopharyngeal  nerve,  18 

lesions  of,  symptoms,  99 
Glossopharyngeovagus,      motor 
pathway  in,  45 

sensory  pathway  of,  59 
Golgi's  cells,  28 
Goll,  funiculus  of,  15 
Graefe's  sign,  194 
Gratiolet's  optic  radiation,  33 
Gray  commiasure,  11 

matter  of  cord,  PI.  52 
structure  of,  29 
Gyrus  fornicatus,  5 

hippocampi,  5 

Hardening,  technic  of,  200 
Headache,  habitual,  163 
Hearing,  testing  of,  118 
Hematoma  of  dura  mater,  136 
Hematonwelia,  175 
Hematorrhachis,  175 
Hemianesthesia,  159 
Hemianopic    pupillarv    rigidity, 

122 
Hemianopsia,  86,  117 
Hemicrania,  102 
Hemiplegia    alternans,     PI.    65, 

Fig.  2 
Hemispheres,    disease   of    mesial 

surface  of,  symptoms,  86 


Hemorrhage,    cerebral,   142  ;   PI. 
62,  Fig.  1 
in  central  canal  of  cord,  175 

Hereditary  ataxia,  105,  185 

Hindbrain,  23 

Huntingdon's  chorea,  166 

Hydrocephalus,  chronic,   PI.  61, 
Fig.  1 
internal,  151 

Hydrotherapy,  134 

Hygienic  treatment,  134 

Hypalgesia,  116 

Hyperemia  of  brain,  141 

Hyperesthesia,  115 
in  hysteria,  159 

Hyperhidrosis,  123 

Hypertrophic  cervical  pachymen- 
ingitis, 167 

Hypesthesia,  115 

Hypnotics,  135 

Hypnotism,  133 

Hypochondria,  158 

Hypoglossal  nerve,  18 

lesions  of,  symptoms,  100 
motor  pathway  of,  46 

Hysteria,  158 
attacks  of,  160 

Hysteric  contractures,  160 
palsies,  159 

Ideation,  67 
Idiopathic  tremor,  166 
Infantile  spinal  paralysis,  181 
Infectious  multiple  neuritis,  193 
Inferior  cerebellar  peduncle,  36 
Infundibulum,  11 
Innervation  feelings,  Q9< 
Insula,  disease  of,  symptoms,  87 
Interbrain,  23 
Intercostal  arteries,  21 

nerves,   lesions   of,    symptoms, 
101 

neuralgia,  190 
Intermediate  neurons,  29 
Internal  capsule,  development  of, 
23 
disease  of,  symptoms,  87 

hydrocephalus,  151 
Intervertebal  ganglion,  19 
Intestines,  sensory  fibers  of,  59 


212 


INDEX. 


Intoxications,  treatment  of,  130 
Intramedullary  fibers,  38 
Island  of  Reil,  4 

Kinesthetic  memory  pictures, 
69 

Lagophthalmos,  99 
Lamina  cornea,  9 
Landry's  paralysis,  193 
Laqueus  superior,  54 
I^ateral  columns  of  cord,  15,  38 

peduncular  fil)ers,  34 

ventricle,  0 
Lenticular  loop,  33 

nucleus,  5,  10 
Leptomeningitis,  acute,  137 
Lingual  monoplegia,  85 
Literal  paraphasia,  125,  127 
Lobe,  frontal,  3 

occipital,  3 

parietal,  3 

temporal,  4 
Lobus  lingualis,  4 
Localization  of  sensations,  115 
Lower  extremity,  motor  pathway 

of,  48 
Lumbar    enlargement    of    cord, 

lesions  of,  symptoms,  94 

Main  en  griffe,  101,  195 
Marchi's  method,  199 
Massage,  134 
Masseter  reflex,  121 
Median  nerye,  lesions  of,   symp- 
toms, 100 
Medical  treatment,  135 
Medulla  oblongata,  14 
development  of,  24 
lesions  of,  symptoms,  90 
positions  of  nuclei  and  course 
of    cranial   nerves  in,   PI. 
23 
secondary  degenerations  in, 
PI.  70^ 
Medullary  canal,  22 
folds,  22 
groove,  22 
sheath,  28 
Medullation,  26 


Medullation,  process  of,  PI.  53 
Membranes,  cerebral,  diseases  of, 

136 
Memory  pictures,  67 

testing,  127 
Meninges,  spinal,  diseases  of,  167 
Meningitis,  basilar,  138 

epidemic     cerebrospinal,    137 ; 

PI.  58 
purulent,  138 
syphilitic,  139 
tubercular,  138  ;  PL  58 
Meningomyelitis,      syphilitic 

spinal,  168 
Mesial  peduncular  fibers,  33 
Microscopic  examination  of  ner- 
vous system,  197 
Midbrain,  23 

Middle  cerebellar  peduncle,  36 
Migraine,  162 
Mind-blindness,  125,  127 
Miosis,  103,  122 
Moebius'  symptom,  194 
Mogigraphia,  188 
Monolexia,  127 
Monophasia,  124,  126 
Monoplegia,  brachial,  85 
crural,  85 
facial,  85 
lingual,  85 
Monro,  foramen  of,  9 
Monticulus,  13 
Moral  treatment,  133 
Morphology  of  nervous  system,  1 
Motor  aphasia,  124 

irritative  symptoms,  examina- 
tion of,  107 
nerves,  diseases  of,  187 
pathway,  40 
of  abducens,  45 
of  bladder,  49 
of  facial  nerve,  45 
of  fifth  nerve,  44 
of  glossopharyngeo\agus,  45 
of  hypoglossus,  46 
of  lower  extremity,  48 
of  oculomotor  nerve,  43 
of  rectum,  49 
of  sexual  organs,  49 
of  spinal  acceasorj'  nerve,  47 


INDEX. 


213 


Motor    pathway   of    sympatlietic 
nerve,  49 
of  trochlear  nerve,  44 
of  upper  extremity,  47 
symptoms  of  disease  of,  81 
peripheral  neurons,   nuclei  of, 

PI.  24 
power,  examination  of,  107 
speech  center,  69 
sphere,  examination  of,  106 
Multiple  cerebrospinal   sclerosis, 
175 
neuritis,  191;  PI.  84 
infectious,  193 
of  pregnancy,  193 
Muscle  sense,  117 

pathway  of,  58 
Muscles,  examination  of,  106 
Muscular  atrophy,  spinal,  PI.  64, 

Fig.  1 
Musculocutaneous  nerve,   lesions 

of,  symptoms,  100 
Mydriasis,  97,  122 
Myelitis,  172  ;  PI.  63,  Fig.  1 
acute  disseminated,  173 
chronic,  PL  63,  Fig.  4 
compression,  169 
dorsalis,  122 
various  forms  of,  PI .  75 
Myelogenic  fibers,  38 
Myeloneuritis,  193 
Myopathy,  primary,  179 
Myotonia  congenita,  166 
Myxedema,  195 

Nerve,  abducens,  18 

auditory,  18 

facial,  18 

glossopharyngeal,  18 

hypoglossal,  18 

oculomotor,  17 

olfactory,  17 

optic,  17 

pneumogastric,  18 

spinal  accessory,  18 

tracts  with  known  functions,  39 
schema  of,  PI.  54-56 

trifacial,  18 

trochlear,  18 
Nerve-cell,  25 


Xerve-fiber,  28 
Nerves,  cranial,  17 

of  pia  and  dura,  21 

peripheral,  17 

spinal,  18 
Nervous  diseases,  causes  of,  75 
pathologic  alterations  in,  78 
symptomatology  of,  81 
topical  diagnosis  of,  81 
treatment  of,  129 

plexuses,  19 

system,  development  of,  22 
morphology  of,  1 
Neuralgia,  189 

trifacial,  190 
Neurasthenia,  157 
Neurilemma,  28 
Neuritis,  acute,  PI.  63,  Fig.  2 

alcoholic,  192 

arsenical,  193 

diphtheric,  192 

multiple,  191  ;  PI.  84 

parenchymatous,  191 

postdiphtheric,  PI.  84,  Fig.  3 

saturnine,  192 
Neuroblasts,  25 
Neuroglia,  development  of,  22,  25 

structure  of,  27 
Neuron,  25,  28 

central  motor,  40 
sensory,  51 

elements,  67 

peripheral  motor,  40 
sensory,  50 
Neurons,  arrangement  of,  PI.  17 
Neuroses,  cerebral,  157 

occupation,  188 

traumatic,  162 
Nucleus,  amygdaloid,  10 

caudate,  5 

globosus,  14 

lenticular,  5,  10 

red,  11 

ruber,  11 

Obex,  15 

Obturator  nerve,  lesions  of,  symp- 
toms, 102 
Occipital  lobe,  3 

disease  of,  symptoms,  86 


214 


INDEX. 


Occipital  nerve,  lesions  of,  symp- 
toms, 100 
neuralgia,  190 
Occipitotemporal  convolution,  4 
Occupation  neuroses,  188 
palsies,  189 
spasms,  188 
Oculomotor  nerve,  17 

lesions  of,  symptoms,  97 
motor  pathway  in,  43 
Olfactory  bulb,  17 
fibrillation,  63 
nerve,  17 

lesions  of,  symptoms,  96 
sensory  pathway  of,  63 
sulcus,  5 
tract,  17 
Olivary  bodies,  15 
Operative  treatment,  131 
Operculum,  4 
Ophthalmoplegia,  104,  154 

chronic  progressive,  PI.  66,  Fig. 
3 
Optic  aphasia,  1 25 
nerve,  17 

lesions  of,  symptoms,  96 
sensory  pathway  of,  62 
thalamus,  11 

disease  of,  symptoms,  88 
tract,  12 
Organic  diseases,  76 
Oval  bundle,  34 

Pacchionian  bodies,  2 
Pachymeningitis,       hypertrophic 
cervical,  167 

internal  hemorrhagic,  136 
Pain  sense,  examination  of,  116 
Palpebral  reflex,  120 
Paracentral  lobule,  4 
Paragraphia,  127 
Paralexia,  126,  127 
Paralysis  agitans,  166 

bulbar,  155 

cerebral,  character  of,  91 

chronic  atrophic  spinal,  182 
bulbar,  PI.  78,  Fig.  1 

Erb's,  96 

infantile  cerebral,  medulla  ob- 
longata in,  PI.  70,  Fig.  2 


Paralysis,  infantile  spinal,  181 
Landry's,  193 
of  lower    portion    of    brachial 

plexus,  96 
plexus,  symptoms  of,  96 
I       progressive,  152 
I       pseudobulbar,  156 

simple  spastic  spinal,  104 
I       spastic,  PI.  65,  Fig.  1 
i  spinal,  176  ;  PI.  81 

Paralytic  dementia,  152 
Paramyoclonus  multiplex,  161 
Paraphasia,  87,  125 
Paraplegia,  flaccid  inferior,  94 
inferior,  85 
universalis,  93 
Parenchymatous  neuritis,  191 
Paresthesias,  113 
Paretic  gait,  108 
Parietal  lobe,  3 

disease  of,  symptoms,  86 
Parieto-occipital  fissure,  4 
Parkinson's  disease,  166 
Passive    motions,    perception   of, 

116 
Patellar  tendon  reflex,  120 
Pathology,  special,  136 
Pathway,  nervous,  39 
Peduncles,  cerebellar,  14 
Pedunculus  conarii,  11 
Perforated  space,  posterior,  16 
Periosteum  reflex,  120 
Peripheral  motor  neuron,  40 

sj^mptom  of  lesion  of,  83 
nerves,  17 
degeneration  of,  PI.  83 
diseases  of,  186 
lesions  of,  symptoms,  95 
neurons,  26 

sensory  neuron  complex,  50 
Peroneal  gait,  108 

nerve,    lesions  of,     symptoms, 
102 
Pes,  5 
\   Pharyngeal  reflex,  120 
Phrenic  nerve,  lesions  of.  symp- 
toms, 100 
Physical  treatment,  134 
Pia  mater,  2 
i   Pial  veins,  21 


INDEX. 


215 


Pineal  gland,  11 
Pituitary  body,  12 

development  of,  24 
Plexus,  choroid,  9 

paralyses,  symptoms  of,  96 
Plexuses,  nervous,  19 
Pli  courbe,  4 
Pneumogastric  nerve,  18 

lesions  of,  symptoms,  99 
Poliomyelitis,  anterior,  104,  180 

chronic,  182 
Polyesthesia,  11 
Polymyositis,  acute,  193 
Polyneuritis,    alcoholic,    PI.    H4, 

Figs.  1  and  2 
Pons,  lesions  of,  symptoms,  89 

secondary  degenerations  of,  PI. 
69 

Varolii,  14 
Position,  sense  of,  117 
Postdiphtheric   neuritis,    PI.    84, 

Fig.  4 
Posterior  columns  of  cord,  15,  38 

commissures,  11 

longitudinal  bundle,  36 
Precuneus,  4 

Primary  cell  diseases,  symptoms 
of,"  104 

diseases,  76 

myopathy,  179 
Primitive  sheath,  28 
Progressive  muscular  dystrophy, 
104,  179 ;  PL  64,  Fig.  4 

paralysis,  152 

spinal  muscular  atrophy,  177 
Projection  fibers,  32 
Propliylaxis,  130 
Protoplasmic  processes,  28 
Pseudobulbar  paralysis,  156 
Pseudohypertrophy,  179 
Psychic  blindness,  86 

functions,  examination  of,  124 

treatment,  133 
Psychoses,  157 
Ptosis,  20,  97 
Pulyinar,  11 
Pupillary  reflex,  121 

arc,  65 
Purulent  meningitis,  138 
Putamen,  10 


Pyramid,  33 
Pyramidal  bodies,  14 
tract,  34,  40 

descending  degenerations  of, 
PI.  71 
Pyramids,  decussation  of,  15 

Radial  nerve,  lesions  of,  symp- 
toms, 100 

reflex,  121 
Reaction  of  degeneration,  110 
Rectum,  examination  of  function 

of,  122 
Red  nucleus,  11 
Reflex,  Achilles  tendon,  121 

arc,  64 
conjunctival,  65 
cutaneous,  64 
pupillary,  65 
tendon,  64 

collateral,  64 

conjunctival,  120 

cremaster,  120 

facial  spasm,  190 

masseter,  121 

palpebral,  120 

patellar  tendon,  120 

paths,  64 

periosteum,  120 

pharyngeal,  120 

pupillary,  121 

radial,  121 

tendon,  120 

triceps  tendon,  121 

ulnar,  121 
Reflexes,  cutaneous.  119 

examination  of.  119 

of  mucous  membranes,  119 
Reil,  island  of,  4 
Restiform  bodies,  14,  15 
Rhinolalia.  124 
Rhomboid  fossa,  13  ;  PI.  10 
Rinn^'s  test,  118 
Rolando,  fissure  of,  3 
Romberg's  phenomenon,  184 

sign,  108 
Roots  of  spinal  nerves,  19 

Sacral  region  of  cord,  lesions  of, 
symptoms,  94 


216 


INDEX. 


Saturnine  neuritis,  192 
Scattered  bundle,  59 
Sciatic  nerve,   lesions  of,   symp- 
toms, 102 
Sciatica,  190 
Sclerose  en  plaques,  175 
Sclerosis,     amyotrophic     lateral, 
177  ;  PL  63,  Fig.  3 
section  of  cord  in,  PL  78, 
Fig.  3 
multiple    cerebrospinal,    175  ; 
PL  77 
Secondary  association    processes, 
67 
atrophy,  79 
degenerations,  79 

in  medulla  oblongata,  PL  70 
of  crusta,  PL  67,  68 
of  pons,  PL  69 
Sedatives,  135 

Sensations,  localization  of,  115 
Sense  of  weight,  examination  of, 

116 
Sensory  aphasia,  86,  125 
impressions,  pathway  of,  57 
nerves,  diseases  of,  189 
pathway,  49 

of  auditory  nerve,  61 
of  glossopharyngeovagus,   59 
of  olfactory  nerve,  63 
of  optic  nerve,  62 
of  trigeminus,  60 
of  vestibular  nerve,  62 
symptoms  of  disease  of,  81,  83 
speech  center,  69 
sphere,  examination  of,  113 
Serial  sections  of  brain  and  coixl, 

PL  28-50 
vSheath  of  Schwann,  28 
Sight,  testing  of,  117 
Simian  fissure,  3 
Singultus,  188 
Sinuses  of  dura  mater,  1 
Sinus-thrombosis,  140 
Smell,  testing  of,  118 
Spasm  of  diaphragm,  188 
of  facial  nerve,  188 
of  mastication,  188 
of  spinal  accessory,  188 
reflex  facial,  190*^ 


Spastic  gait,  108 

spinal  paralysis,  176  ;  PL  81 
torticollis,  188 
Special  pathology,  136 
Speech,  examination  of,  124 

path,  47 
Spinal  accessory  nerve,  18 

lesions  of,  symptoms,  100 
motor  pathway  in,  47 
spasm  of,  188 
cord,  anatomy  of,  15 
arteries  of,  20 
ascending    degeneration    of, 

PL  73 
columns  of,  15,  16,  38 
compression  of,  169 
course  of  fibers  in,  PL  57 
descending  degeneration   of, 

PL  72 
diseases  of,  167 
symptoms,  92 
gray  matter  of,  PL  52 
hemorrhages  in  central  canal 

of,  175 
sections  of,  PL  14 
meninges,  diseases  of,  167 
meningomyelitis,  168 
muscular  atrophy,  104 

progressive,  177 
nerves,  18 

development  of,  26 
distribution  of,  PL  27 
paralysis,  simple  spastic,  104 
spastic,  176 
Spindle  cells,  25 
Splenium,  5 
Stammering,  124 
Static  coordination,  108 
Status  epilepticus,  164 
Stigmata,  hysteric.  158 
Stratum  zonale,  32 
Stria  pinealis,  11 
Striae  acusticse,  14 
St.  Vitus  dance,  165 
Subarachnoid  space,  2 
Subjective    symptoms,    examina- 
tion of,  113 
Substantia  nigra,  12 
Subthalamic    region,    lesion    of, 
symptoms,  88 


INDEX. 


217 


Sulci,  cerebral,  3 
Sulcus,  central,  3 
olfactory,  5 
rectus.  5 
Supramarginal  convolution,  4 
Surgical  operations,  131 
Sydenham's  chorea,  165 
Sylvius,  aqueduct  of,  1:2 

fiasure  of.  4 
Sympathetic    nerve,    lesions    of, 
symptoms,  103 
motor  pathway  of.  49 
Symptomatic  treatment,  133 
Symptomatology  of  nervous  dis- 
eases, HI 
Symptoms  of  cortical  lesions,  84 
of  focal  diseases,  84 
of  system  diseases,  103 
Syphilis,  brain,  139 
Syphilitic  cases,  treatment,  131 
meningitis,  139 
spinal  meningomyelitis,  168 
Syringomyelia,  174*;  PI.  76 
System  disease,  78 

centripetal      sensory      path, 

symptoms,  105 
combined,  symptoms,  105 
corticomuscular  motor  path, 

104 
spinal  cord,  176 
symptoms  of,  103 

Tabes  combine,  105 

dorsalis,  105,  182  ;  PI.  79,  80 

olfactorum,  17 
Tactile  sense,  examination  of,  113 

pathway  of,  58 
Taenia  medullaris,  11 
Tapetum,  30 

Taste,  examination  of,  119 
Tegmental  fibers  of  corona  radi- 

ata,  33 
Tegmentum,  12 

ventriculorum,  6 
Tela  choroidea  inferior,  2 

superior,  9 
Teleneuron,  40 
Temperature  sense,    examination 

of,  116 
Temporal  lobe,  4 


Tendon  reflex  arc,  64 

reflexes,  120 
Tentorium,  2 
Tetanus,  196 
Tetany,  195 
Thalamus,  optic,  11 
Thermo-anesthesia,  116 
Third  ventricle,  9 
Thomsen's  disease,  166 
Thoracic  nerve,  lesions  of,  symp- 
toms, 100 

region  of  cord,  lesions  of,  symp- 
toms, 94 
Thrombosis,  brain,  145 

of  sinuses,  140 
Tibial    nerve,   lesions   of,    symp- 
toms, 103 
Tic  convulsif,  188 

douloureux,  190 
Tonic  spasm,  107 
Tonsilla,  14 

Topographic   sense,   examinatiou 
-  of,  115 

Torticollis,  spastic,  188 
Tract  of  crusta,  33 

of  fillet,  33 

pyramidal,  34 
Traumatic  neuroses,  162 
Treatment,  129 

hygienic,  134 

medical,  135 

moral,  133 

physical,  134 

psychic,  133 

special,  136 

symptomatic,  133 
Tremor,  examination  of,  107 

idiopathic,  166 
Triceps  tendon  reflex,  121 
Trifacial  nerve,  18 

lesions  of,  symptoms,  97 

neuralgia,  190 
Trigeminus,  sensory  pathway  of, 

60 
Trigonum  habenulae,  11 
Triradiate  fissure,  5 
Trismus,  188 
Trochlear  nerve,  18 

lesions  of,  symptoms,  97 
motor  pathway  in,  44 


218 


INDEX. 


Trophic  disturbances,  examina- 
tion of,  123 

Trousseau's  phenomenon,  195 

Tubercular  nieninjjitis,  13H  ;  PI. 
58 

Tumor  of  brain,  149;  PI.  59,  Fig.  3 
of  pons,  PI.  60,  Fig.  2 ;  PI.  66, 
Fig.  2 

Tiirck's  bundle,  34 

Ulnar  nerve,  lesions  of,    symp- 
toms, 101 

reflex,  121 
Unconscious  associations,  68 
Upper  extremity,  motor  pathway 

of,  47 

Vasomotor  disturbances,  exami- 
nation of,  123 

Velum  interpositum,  9 

Venous  sinuses,  1 

Ventricle,  fifth,  8 
fourth,  13 
lateral,  6 


Ventricle,  third,  9 
Ventricles,  cerebral,  6 
Ventricular     system    of      brain, 

schema  of,  PI.  H 
Vermiform  ]>rocess,  12 
Vermis,  12 
Vertebral  arteries,  20 
Vestibular     nerve,     lesions      of, 
symptoms,  99 
sensory  pathway  of,  62 
Visual  aphasia,  86 

impressions,  storing  up  of,  67 
Volitional  pathways,  66 

Wagner  hammer.  111 
Westphal's  sign,  184 
White  matter,  structure  of,  29 
Willis,  circle  of,  20 
Word-deafness,  125 
Word-sound  center,  69 
Wrist-drop,  101 
Writer's  cramp,  188 
Writing,  examination  of,  127 
Wry  neck,  100 


of 


Catalogue    tt    Medical     Publications 


OF 


W.   B.  SAUNDERS   &   COMPANY 

PHILADELPHIA       ^        ^        jIt        ^        j»  LONDON 

925  Walnut  Street    ^       ^        ^        ^        ^    161  Strand,  W.  C. 

Arranged  Alphabetically  and  Classified  under  Subjects 
See  page  18  for  a  List  of  Contents  classified  according  to  subjects 

THE  books  advertised  in  this  Catalogue  as  being  sold  by  subscription  are  usually  to  be 
obtained  from  travelling  solicitors,  but  they  will  be  sent  direct  from  the  office  of  pub- 
lication (charges  of  shipment  prepaid)  upon  receipt  of  the  prices  given.     All  the  other 
books  advertised  are  commonly  for  sale  by  booksellers  in  all  parts  of  the  United  States ;  but 
books  will  be  sent  to  any  address,  carriage  prepaid,  on  receipt  of  the  published  price. 

Money  may  be  sent  at  the  risk  of  the  publisher  in  either  of  the  following  ways  :  A  postal 
money  order,  an  express  money  order,  a  bank  check,  and  in  a  registered  letter.  Money 
sent  in  any  other  way  is  at  the  risk  of    the  sender. 

SPECIAL  To  physicians  of  approved  credit  books  will  be  sent,  post-paid,  on  the  following 
OFFER  terms  :  $5.00  cash  upon  delivery  of  books,  and  monthly  payments  of  #5.00  there- 
after until  full  amount  is  paid.  Physicians  not  known  to  the  house  will  be  expected  to  furnish 
the  names  of  satisfactory  references.  Any  one  or  two  volumes  will  be  sent  on  thirty  days' 
time  to  those  who  do  not  care  to  make  a  larger  purchase. 


AN  AMERICAN  TEXT-BOOK  OF  APPLIED  THERAPEUTICS. 

Edited  by  JAMES  C.  WiLSON,  M.  D.,  Professor  of  Practice  of  Medicine  and 
of  Clinical  Medicine,  Jefferson  Medical  College,  Philadelphia.  Handsome 
imperial  octavo  volume  of  1326  pages.  Illustrated.  Cloth,  ^7.00  net; 
Sheep  or  Half  Morocco,  ^8.00  net.     Sold  by  Subscription. 

AN  AMERICAN  TEXT=BOOK  OF  THE   DISEASES  OF  CHIL- 
DREN.   Second  Edition,  Revised. 

Edited  by  LouiS  STARR,  M.  D.,  Consulting  Pediatrist  to  the  Maternity  Hos- 
pital, etc.  ;  assisted  by  THOMPSON  S.  Westcott,  M.D.,  Attending  Physi- 
cian to  the  Dispensary  for  Diseases  of  Children,  Hospital  of  the  University 
of  Pennsylvania.  Handsome  imperial  octavo  volume  of  1244  pages,  pro- 
fusely illustrated.  Cloth,  $7.00  net ;  Sheep  or  Half  Morocco,  ^8.00  net. 
Sold  by  Subscription. 

AN  AMERICAN   TEXT=BOOK  OF   DISEASES  OF  THE   EYE, 
EAR,  NOSE,  AND  THROAT. 

Edited  by  G.  E,  DE  SCHWEINITZ,  M.  D.,  Professor  of  Ophthalmology, 
Jefferson  Medical  College,  Philadelphia ;  and  B.  Alexander  Randall^ 
"M.  D.,  Professor  of  Diseases  of  the  Ear,  University  of  Pennsylvania. 
Imperial  octavo,  1251  pages;  766  illustrations,  59  of  them  in  colors. 
Cloth,  ^7.00  net ;  Sheep  or  Half  Morocco,  ^8.00  net.     Sold  by  Subscription. 


MEDICAL    PUBLICATIONS 


AN    AMERICAN    TEXT=BOOK    OF    QENITO=URINARY    AND 
SKIN  DISEASES. 

Edited  by  L.  BoLTON  Bangs,  M.  D.,  Professor  of  Genito-Urinary  Surgery, 
University  and  Bellevue  Hospital  Medical  College,  New  York;  and  W.  A. 
Hardaway,  M.  D.,  Professor  of  Diseases  of  the  Skin,  Missouri  Medical 
College.  Imperial  octavo  volume  of  1229  pages,  with  300  engravings  and 
20  full-page  colored  plates.  Cloth,  ^7.00  net;  Sheep  or  Half  Morocco, 
^8.00  net.     Sold  by  Subscription. 

AN    AMERICAN   TEXT=BOOK   OF   GYNECOLOGY,   MEDICAL 
ANP  SURGICAL.    Second  Edition,  Revised. 

Edited  by  J.  M.  Baldy,  M.  D.,  Professor  of  Gynecology,  Philadelphia 
Polyclinic,  etc.  Handsome  imperial  octavo  volume  of  718  pages  ;  341  illus- 
trations in  the  text,  and  38  colored  and  half-tone  plates.  Cloth,  j^6.oo  net ; 
Sheep  or  Half  Morocco,  ^7.00  net.     Sold  by  Subscription. 

AN    AMERICAN    TEXT=BOOK   OF    LEGAL    MEDICINE    AND 
TOXICOLOGY. 

Edited  by  Frederick  Peterson,  M.  D.,  Chief  of  Clinic,  Nervous  Depart- 
ment, College  of  Physicians  and  Surgeons,  New  York  ;  and  Walter  S. 
Haines,  M.  D.,  Professor  of  Chemistry,  Pharmacy,  and  Toxicology,  Rush 
Medical  College,  Chicago.     In  Preparation. 

AN  AMERICAN  TEXT=BOOK  OF  OBSTETRICS. 

Edited  by  Richard  C.  Norris,  M.  D.  ;  Art  Editor,  Robert  L.  Dickinson, 
M.  D,  Handsome  imperial  octavo  volume  of  1014  pages  ;  nearly  900  beau- 
tiful colored  and  half-tone  illustrations.  Cloth,  ^7.00  net ;  Sheep  or  Half 
Morocco,  ^8.00  net.     Sold  by  Subscription. 

AN  AMERICAN  TEXT=BOOK  OF  PATHOLOGY. 

Edited  by  LUDWIG  Hektoen,  M.  D.,  Professor  of  Pathology  in  Rush 
Medical  College,  Chicago  ;  and  David  Riesman,  M.  D.,  Demonstrator  of 
Pathologic  Histology  in  the  University  of  Pennsylvania.  In  Press,  Ready 
Shortly. 

AN  AMERICAN  TEXT=BOOK  OF  PHYSIOLOGY.     Second  Edi- 
tion, Revised,  in  Two  Volumes. 

Edited  by  WILLIAM  H.  HoWELL,  Ph.  D.,  M.  D.,  Professor  of  Physiology, 
Johns  Hopkins  University,  Baltimore,  Md.  Two  royal  octavo  volumes  of 
about  600  pages  each.  Fully  illustrated.  Per  volume:  Cloth,  ^3.00  net; 
Sheep  or  Half  Morocco,  $3.75  net. 

AN  AMERICAN  TEXT=BOOK  OF  SURGERY.    Third  Edition. 

Edited  by  WILLIAM  W.  Keen,  M.  D.,  LL.D.,  F.  R.  C.  S.  (Hon.);  and 
J.  William  White,  M.  D.,  Ph.  D.  Handsome  octavo  volume  of  1230 
pages  ;  496  wood-cuts  and  37  colored  and  half-tone  plates.  Thoroughly 
revised  and  enlarged,  with  a  section  devoted  to  "The  Use  of  the  Ront- 
gen  Rays  in  Surgery."  Cloth,  ;^7.oo  net ;  Sheep  or  Half  Morocco, 
58.00  net, 


OF  W.  B.   SAUNDERS  &-  CO. 


THE  NEW  STANDARD  THE  NEW  STANDARD 

THE  AMERICAN  ILLUSTRATED  MEDICAL  DICTIONARY. 

For  Practitioners  and  Students.  A  Complete  Dictionary  of  the  Terms  used 
in  Medicine,  Surgery,  Dentistry,  Pharmacy,  Chemistry,  and  the  kindred 
branches,  including  much  collateral  information  of  an  encyclopedic  character, 
together  with  new  and  elaborate  tables  of  Arteries,  Muscles,  Nerves,  Veins, 
etc.  ;  of  BaciUi,  Bacteria,  Micrococci,  Streptococci ;  Eponymic  Tables  of 
Diseases,  Operations,  Signs  and  Symptoms,  Stains,  Tests,  Methods  of  Treat- 
ment, etc.,  etc.  By  W.  A.  NEWMAN  Dorland,  A,  M.,  M.  D.,  Editor 
of  the  "  American  Pocket  Medical  Dictionary."  Handsome  large  octavo, 
nearly  800  pages,  bound  in  full  flexible  leather.  Price,  ^4.50  net ;  with 
thumb  index,  ^5.00  net. 


Gives  a  Maximum  Amount  of  Matter  in  a  Minimum  Space  and  at  the  Lowest 
Possible  Cost. 

This  is  an  entirely  new  and  unique  work,  intended  to  meet  the  need  of  practitioners  and 
students  for  a  complete  up-to-date  dictionary  of  moderate  price.  It  contains  more  than  twice 
the  material  in  the  ordinary  students'  dictionary,  and  yet,  by  the  use  of  a  clear,  condensed 
type  and  thin  paper  of  the  finest  quality,  it  forms  an  extremely  handy  volume  only  1%  inches 
in  thickness.  It  is  a  beautiful  specimen  of  the  bookmaker's  art.  It  is  bound  in  full  flexible 
leather,  and  is  just  the  kind  of  book  that  a  man  will  want  to  keep  on  his  desk  for  constant 
reference.  The  book  makes  a  special  feature  of  the  newer  words,  and  defines  hundreds  of 
important  terms  not  to  be  found  in  any  other  dictionary.  It  is  especially  full  in  the  matter 
of  tables,  containing  more  than  a  hundred  of  great  practical  value.  An  important  feature 
of  the  book  is  its  handsome  illustrations  and  colored  plates  drawn  especially  for  the  work, 
including  new  colored  plates  of  Arteries,  Nerves,  Veins,  Bacteria,  Blood,  etc. — twenty-four  in 
all.     This  new  work  has  been  aptly  termed  by  a  competent  critic  "  The  New  Standard." 

THE  AMERICAN    POCKET    MEDICAL    DICTIONARY.    Third 
Edition,  Revised. 

Edited  by  W.  A.  NEWMAN  DoRLAND.,  M.  D.,  Assistant  Obstetrician  to  the 
Hospital  of  the  University  of  Pennsylvania ;  Fellow  of  the  American  Acad- 
emy of  Medicine.  Containing  the  pronunciation  and  definition  of  the  prin- 
cipal words  used  in  medicine  and  kindred  sciences,  with  64  extensive  tables. 
Handsomely  bound  in  flexible  leather,  with  gold  edges.  Price  ^i. 00  net; 
with  thumb  index,  $1.25  net. 

THE  AMERICAN  YEAR=BOOK  OF  MEDICINE  AND  SURGERY. 

A  Yearly  Digest  of  Scientific  Progress  and  Authoritative  Opinion  in  all 
branches  of  Medicine  and  Surgery,  drawn  from  journals,  monographs,  and 
text-books  of  the  leading  American  and  Foreign  authors  and  investigators. 
Arranged  with  editorial  comments,  by  eminent  American  specialists,  under 
the  editorial  charge  of  George  M.  Gould,  M.  D.  Year-Book  of  1901 
in  two  volumes — Vol.  I.  including  General  Medicine  ;  Vol.  II.,  General  Sur- 
gery. Per  volume  :  Cloth,  ^3.00  net ;  Half  Morocco,  $3.75  net.  Sold  by  Sub- 
scription. 

ABBOTT  ON  TRANSMISSIBLE  DISEASES. 

The  Hygiene  of  Transmissible  Diseases:  their  Causation,  Modes  of  Dissem- 
ination, and  Methods  of  Prevention.  By  A.  C.  ABBOTT,  M.  D.,  Professor 
of  Hygiene  and  Bacteriology,  University  of  Pennsylvania.  Octavo,  311  pages, 
with  numerous  illustrations.     Cloth,  ^2.00  net. 


MEDICAL   PUB  Lie  A  TIONS 


ANDERS'  PRACTICE  OF  MEDICINE.    Fourth  Revised  Edition. 

A  Text-Book  of  the  Practice  of  Medicine,  By  James  M.  Anders,  M.  D,, 
Ph.  D.,  LL.  D.,  Professor  of  the  Practice  of  Medicine  and  of  Clinical  Med- 
icine, Medico-Chirurgical  College,  Philadelphia.  Handsome  octavo  volume 
of  1292  pages,  fully  illustrated.  Cloth,  $5.50  net;  Sheep  or  Half  Morocco, 
^6.50  net. 

BASTIN'S  BOTANY. 

Laboratory  Exercises  in  Botany.  By  Edson  S.  Bastin,  M.  A.,  late  Pro- 
fessor of  Materia  Medica  and  IBotany,  Philadelphia  College  of  Pharmacy. 
Octavo,  536  pages,  with  87  plates.     Cloth,  ^2.00  net. 

BECK  ON  FRACTURES. 

Fractures.  By  Carl  Beck,  M.  D.,  Surgeon  to  St.  Mark's  Hospital  and 
the  New  York  German  Poliklinik,  etc.  With  an  appendix  on  the  Practical 
Use  of  the  Rontgen  Rays.     335  pages,  170  illustrations.     Cloth,  ^^3.50  net. 

BECK'S  SURGICAL   ASEPSIS. 

A  Manual  of  Surgical  Asepsis.  By  Carl  Beck,  M.  D.,  Surgeon  to  St. 
Mark's  Hospital  and  the  New  York  German  Poliklinik,  etc.  306  pages;  65 
text-illustrations  and  12  full-page  plates.     Cloth,  ^1.25  net. 

BOISLINIERE'S    OBSTETRIC    ACCIDENTS,    EMERGENCIES, 
AND  OPERATIONS. 

Obstetric  Accidents,  Emergencies,  and  Operations.  By  L.  Ch.  Boislin- 
iere,  M.  D.,  late  Emeritus  Professor  of  Obstetrics,  St.  Louis  Medical  Col- 
lege.    381  pages,  handsomely  illustrated.     Cloth,  |s2.oo  net. 

BOHM,   DAVIDOFF,   AND   HUBER'S   HISTOLOGY. 

A  Text-Book  of  Human  Histology.  Including  Microscopic  Technic.  By 
Dr.  a.  a.  Bohm  and  Dr.  M.  v6n  Davidoff,  of  Munich,  and  G.  Carl 
HUBER,  M.  D.,  Junior  Professor  of  Anatomy  and  Director  of  Histological 
Laboratory,  University  of  Michigan.  Handsome  octavo  of  501  pages,  with 
351  beautiful  original  illustrations.     Cloth,  $3.50  net. 

BUTLER'S      MATERIA      MEDICA,     THERAPEUTICS,     AND 
PHARMACOLOGY.    Third  Edition,  Revised. 

A  Text-Book  of  Materia  Medica,  Therapeutics,  and  Pharmacology.  By 
George  F.  Butler,  Ph.  G.,  M.  D.,  Professor  cf  Materia  Medica  and  of 
Clinical  Medicine,  College  of  Physicians  and  Surgeons,  Chicago.  Octavo, 
874  pages,  illustrated.    Cloth,  ^4.00  net ;  Sheep  or  Half  Morocco,  $5.00  net. 

CERNA    ON    THE    NEWER     REMEDIES.       Second     Edition, 
Revised. 

Notes  on  the  Newer  Remedies,  their  Therapeutic  Applications  and  Modes 
of  Administration.  By  David  Cerna,  M.  D.,  Ph.  D.,  Demonstrator  of 
Physiology,  Medical  Department,  University  of  Texas.  Rewritten  and 
greatly  enlarged.     Post-octavo,  253  pages.     Cloth,  ;^i.oo  net. 


OF   W.  B.  SAUNDERS  &-   CO. 


CHAPIN  ON  INSANITY. 

A  Compendium  of  Insanity.  By  John  B.  Chapin,  M.  D.,  LL.D.,  Phy- 
sician-in-Chief,  Pennsylvania  Hospital  for  the  Insane;  Honorary  Member 
of  the  Medico-Psychological  Society  of  Great  Britain,  of  the  Society  of 
Mental  Medicine  of  Belgium,  etc.  i2mo,  234  pages,  illustrated.  Cloth, 
^1.25  net. 

CHAPMAN'S  MEDICAL  JURISPRUDENCE  AND  TOXICOLOGY. 
Second  Edition,  Revised. 

Medical  Jurisprudence  and  Toxicology.  By  HENRY  C.  CHAPMAN,  M.  D.. 
Professor  of  Institutes  of  Medicine  and  Medical  Jurisprudence,  Jefferson 
Medical  College  of  Philadelphia.  254  pages,  with  55  illustrations  and  3 
full-page  plates  in  colors.     Cloth,  ^1.50  net. 

CHURCH  AND  PETERSON'S  NERVOUS  AND  MENTAL  DIS= 
EASES.    Second  Edition. 

Nervous  and  Mental  Diseases.  By  ARCHIBALD  CHURCH,  M.  D.,  Pro- 
fessor of  Nervous  and  Mental  Diseases,  and  Head  of  the  Neurological 
Department.  Northwestern  University  Medical  School,  Chicago ;  and 
Frederick  Peterson,  M.  D.,  Chief  of  Chnic,  Nervous  Department,  Col- 
lege of  Physicians  and  Surgeons,  New  York.  Handsome  octavo  volume  of 
843  pages,  profusely  illustrated.  Cloth,  $5.00  net ;  Sheep  or  Half  Morocco. 
^6.00  net. 

CLARKSON'S  HISTOLOGY. 

A  Text-Book  of  Histology,  Descriptive  and  Practical.  By  Arthur  Clark- 
SON,  M.  B.,  C.  M.  Edin.,  formerly  Demonstrator  of  Physiology  in  the  Owen's 
College,  Manchester  ;  late  Demonstrator  of  Physiology  in  Yorkshire  College, 
Leeds.  Large  octavo,  554  pages  ;  22  engravings  and  174  beautifully  colored 
original  illustrations.     Cloth,  ^.00  net. 

CORWIN'S  PHYSICAL  DIAGNOSIS.    Third  Edition,  Revised. 

Essentials  of  Physical  Diagnosis  of  the  Thorax.  By  ARTHUR  M.  CORWIN, 
A.M.,  M.D.,  Instructor  in  Physical  Diagnosis  in  Rush  Medical  College, 
Chicago.     219  pages,  illustrated.     Cloth,  ^1.25  net. 

CROOKSHANK'S  BACTERIOLOGY.     Fourth  Edition,  Revised. 

A  Text-Book  of  Bacteriology.  By  Edgar  M.  Crookshank,  M.  B.,  Pro- 
fessor of  Comparative  Pathology  and  Bacteriology.  King's  College,  London. 
Octavo,  700  pages,  273  engravings  and  22  original  colored  plates.  Cloth, 
$6.50  net ;   Half  Morocco,  $7.50  net. 

DACOSTA'S  SURGERY.    Third  Edition,  Revised. 

Modern  Surgery,  General  and  Operative.  By  John  CHALMERS  DaCosta, 
M.  D.,  Professor  of  Principles  of  Surgery  and  Clinical  Surgery,  Jefferson 
Medical  College,  Philadelphia  ;  Surgeon  to  the  Philadelphia  Hospital,  etc. 
Handsome  octavo  volume  of  1117  pages,  profusely  illustrated.  Cloth,  ^^5.00 
net ;  Sheep  or  Half  Morocco,  $6.00  net. 

Enlarged  by  over  200  Pages,  with  more  than  100  New  Illus- 
trations. 


MEDICAL    PUBLICATIONS 


DAVIS'S  OBSTETRIC  NURSING. 

Obstetric  and  Gynecologic  Nursing.  By  Edward  P.  Da\is,  A.  M.,  M.  D., 
Professor  of  Obstetrics  in  Jefferson  Medical  College  and  the  Philadelphia 
Polyclinic ;  Obstetrician  and  Gynecologist  to  the  Philadelphia  Hospital. 
i2mo  volume  of  400  pages,  fully  illustrated.     Crushed  buckram,  ^1.75  net. 

DESCHWEINITZ  ON  DISEASES  OF  THE  EYE.    Third  Edition, 
Revised. 

Diseases  of  the  Eye.  A  Handbook  of  Ophthalmic  Practice,  By  G.  E. 
DE  SCHWEINITZ,  M.  D.,  Professor  of  Ophthalmology,  Jefferson  Medical 
College,  Philadelphia,  etc.  Handsome  royal  octavo  volume  of  696  pages ; 
256  fine  illustrations  and  2  chromo-lithographic  plates.  Cloth,  ^4.00  net ; 
Sheep  or  Half  Morocco,  ^5.00  net. 

DORLAND'S  DICTIONARIES. 

[See  American  Illustrated  Medical  Dictionary  and  Ameri can- 
Pocket  Medical  Dictionary  on  page  3.] 

DORLAND»S  OBSTETRICS. 

A  Manual  of  Obstetrics.  By  W.  A.  NEWMAN  BORLAND,  M.  D.,  Assistant 
Demonstrator  of  Obstetrics,  University  of  Pennsylvania  ;  Associate  in  Gyne- 
cology, Philadelphia  Polyclinic.  760  pages;  163  illustrations  in  the  text  and 
6  full-page  plates.     Cloth,  ^^2.50  net. 

EICHHORST'S  PRACTICE  OF  MEDICINE. 

A  Te.xt-Book  of  the  Practice  of  Medicine.  By  Dr.  Herman  Eichhorst, 
Professor  of  Special  Pathology  and  Therapeutics  and  Director  of  the  Medi- 
cal Clinic,  University  of  Zurich.  Translated  and  edited  by  AUGUSTUS  A. 
E^SHNER,  M.  D.,  Professor  of  Clinical  Medicine,  Philadelphia  Polyclinic. 
In  Press.     Ready  Soon. 

FRIEDRICH  AND  CURTIS  ON  THE  NOSE,  THROAT,  AND 
EAR. 

Rhinology,  Laryngology,  and  Otology,  and  their  Significance  in  General 
Medicine.  By  Dr.  E.  P.  Friedrich,  of  Leipzig.  Edited  by  H .  HOLBROOK 
Curtis,  M.  D.,  Consulting  Surgeon  to  the  New  York  Nose  and  Throat  Hos- 
pital.    Octavo,  348  pages.     Cloth,  ^^2.50  net. 

FROTHINQHAM'S  GUIDE  FOR  THE  BACTERIOLOGIST. 

Laboratory  Guide  for  the  Bacteriologist.  By  Langdon  Frothingham, 
M.  D.  v..  Assistant  in  Bacteriology  and  Veterinary  Science,  Sheffield  Scien- 
tific School,  Yale  University.     Illustrated.     Cloth,  75  cts.  net. 

GARRIGUES'    DISEASES    OF    WOMEN.     Third  Edition,   Re- 
vised. 

Diseases  of  Women.  By  Henry  J.  Garrigues,  A.  M.,  M.  D.,  Gynecolo- 
gist to  St.  Mark's  Hospital  and  to  the  German  Dispensary,  New  York  City. 
Octavo,  756  pages,  with  367  engravings  and  colored  plates.  Cloth,  I4.50 
net ;  Sheep  or  Half  Morocco,  ^^5.50  net. 


OF  W.  B.  SAUNDERS  ^  CO. 


GOULD  AND  PYLE'S  CURIOSITIES  OF  MEDICINE. 

Anomalies  and  Curiosities  of  Medicine.  By  GEORGE  M.  GoULD,  M.  D., 
and  Walter  L.  Pyle,  M,  D,  An  encyclopedic  collection  of  rare  and  ex- 
traordinary cases  and  of  the  most  striking  instances  of  abnormality  in  all 
branches  of  Medicine  and  Surgery,  derived  from  an  exhaustive  research  of 
medical  literature  from  its  origin  to  the  present  day,  abstracted,  classified, 
annotated,  and  indexed.  Handsome  octavo  volume  of  968  pages  ;  295  en- 
gravings and  12  full-page  plates.  Popular  Edition.  Cloth,  $3.00  net ;  Sheep 
or  Half  Morocco,  $4.00  net. 

QRAFSTROM'S  MECHANO-THERAPY. 

A  Text-Book  of  Mechano-Therapy  (Massage  and  Medical  Gymnastics). 
By  Axel  V.  Grafstrom,  B.  Sc,  M.  D.,  late  House  Physician,  City  Hos- 
pital, Blackwell's  Island,  New  York.  i2mo,  139  pages,  illustrated.  Cloth, 
^i.oo  net. 

GRIFFITH  ON  THE  BABY.    Second  Edition,  Revised. 

The  Care  of  the  Baby.  By  J.  P.  Crozer  GRIFFITH,  M.  D.,  Clinical  Pro- 
fessor of  Diseases  of  Children,  University  of  Pennsylvania  ;  Physician  to  the 
Children's  Hospital,  Philadelphia,  etc.  i2mo,  404  pages,  67  illustrations 
and  5  plates.     Cloth,  ^1.50  net. 

GRIFFITH'S  WEIGHT  CHART. 

Infant's  Weight  Chart.  Designed  by  J.  P.  Crozer  GRIFFITH,  M.  D., 
Clinical  Professor  of  Diseases  of  Children,  University  of  Pennsylvania.  25 
charts  in  each  pad.     Per  pad,  50  cts.  net. 

HART'S  DIET  IN  SICKNESS  AND  IN  HEALTH. 

Diet  in  Sickness  and  Health.  By  Mrs.  Ernest  Hart,  formerly  Student 
of  the  Faculty  of  Medicine  of  Paris  and  of  the  London  School  of  Medicine 
for  Women  ;  with  an  Introduction  by  SIR  Henry  Thompson,  F.  R.  C.  S., 
M.  D.,  London.     220  pages.     Cloth.  $1.50  net. 

HAYNES'   ANATOMY. 

A  Manual  of  Anatomy.  By  IRVING  S.  Haynes,  M.  D.,  Professor  of  Prac- 
tical Anatomy  in  Cornell  University  Medical  College.  680  pages ;  42  dia- 
grams and  134  full-page  half-tone  illustrations  from  original  photographs  of 
the  author's  dissections.     Cloth,  $2.50  net. 

HEISLER'S  EMBRYOLOGY. 

A  Text-Book  of  Embryology.  By  JOHN  C.  Heisler,  M.  D.,  Professor  of 
Anatomy,  Medico-Chirurgical  College,  Philadelphia.  Octavo  volume  of  405 
pages,  handsomely  illustrated.     Cloth,  ^2.50  net. 

HIRST'S  OBSTETRICS.    Second  Edition. 

A  Text-Book  of  Obstetrics.  By  BARTON  CoOKE  Hirst,  M.  D.,  Professor 
of  Obstetrics,  University  of  Pennsylvania.  Handsome  octavo  volume  of  848 
pages  ;  618  illustrations  and  7  colored  plates.  Cloth,  ^5.00  net  ;  Sheep  or 
Half  Morocco,  ^6.00  net. 


MEDICAL   PUB  Lie  A  TIONS 


HYDE  &  MONTGOMERY  ON  SYPHILIS  AND  THE  VENEREAL 
DISEASES.    3d  Edition,  Revised  and  Greatly  Enlarged. 

Syphilis  and  the  Venereal  Diseases.  By  jAMES  Nevins  Hyde,  M.  D.,  Pro- 
fessor of  Skin  and  Venereal  Diseases,  and  Frank  H.  Montgomery,  M.  D., 
Associate  Professor  of  Skin,  Genito-Urinary,  and  Venereal  Diseases  in  Rush 
Medical  College,  Chicago,  111.  Octavo,  594  pages,  profusely  illustrated. 
Cloth,  ^4.00  net. 

THE  INTERNATIONAL  TEXT-BOOK  OF  SURGERY.     In  Two 
Volumes. 

By  American  and  British  Authors.     Edited  by  J.  COLLINS  Warren,  M,  D., 

LL.  D.,  F.  R.C.  S.  (Hon.),  Professor  of  Surgery,  Harvard  Medical  School, 

Boston  ;  and  A.  Pearce  Gould,  M.  S.,  F.  R.  C.  S.,  Lecturer  on  Practical 

Surgery  and  Teacher  of  Operative  Surgery,  Middlesex  Hospital  Medical 

School,  London,   Eng.     Vol.  L   General  Surgery. — Handsome  octavo,  947 

pages,  with  458  beautiful  illustrations  and  9  Hthographic  plates.     Vol.  H. 

Special  or  Regional  Surgery. — Handsome  octavo,    1072   pages,  with  471 

beautiful    illustrations    and   8    lithographic    plates.      Sold  by   Subscription. 

Prices  per  volume  :  Cloth,  ^5.00  net :  Sheep  or  Half  Morocco,  $6.00  net. 

"  It  is  the  most  valuable  work  on  the  subject  that  has  appeared  in  some  years.     The 

clinician  and  the  pathologist  have  joined  hands  in  its  production,  and  the  result  must  be  a 

satisfaction  to  the  editors  as  it  is  a  gratification  to  the  conscientious  reader." — Annals  of 

Surgery. 

"  This  is  a  work  which  comes  to  us  on  its  own  intrinsic  merits.  Of  the  latter  it  has 
very  many.  The  arrangement  of  subjects  is  excellent,  and  their  treatment  by  the  different 
authors  is  equally  so.  What  is  especially  to  be  recommended  is  the  painstaking  endeavor 
of  each  writer  to  make  his  subject  clear  and  to  the  point.  To  this  end  particularly  is  the 
technique  of  operations  lucidly  described  in  all  necessary  detail.  And  withal  the  work  is  up 
to  date  in  a  very  remarkable  degree,  many  of  the  latest  operations  in  the  different  regional 
parts  of  the  body  being  given  in  full  details.  There  is  not  a  chapter  in  the  work  from  which 
the  reader  may  not  learn  something  new." — Aledical  Record,  New  York. 

JACKSON'S  DISEASES  OF  THE  EYE. 

A  Manual  of  Diseases  of  the  Eye.  By  Edward  Jackson,  A.M.,  M.  D., 
Emeritus  Professor  of  Diseases  of  the  Eye,  Philadelphia  PolycHnic  and  Col- 
lege for  Graduates  in  Medicine.  i2mo,  volume  of  535  pages,  with  178  illus- 
trations, mostly  from  drawings  by  the  author.     Cloth,  $2.50  net. 

KEATING'S  LIFE  INSURANCE. 

How  to  Examine  for  Life  Insurance.  By  JOHN  M.  Keating,  M.  D.,  Fellow 
of  the  College  of  Physicians  of  Philadelphia  ;  Ex-President  of  the  Association 
of  Life  Insurance  Medical  Directors.  Royal  octavo,  211  pages.  With 
numerous  illustrations.     Cloth,  ^2.00  net. 

KEEN  ON  THE  SURGERY  OF  TYPHOID  FEVER. 

The  Surgical  Complications  and  Sequels  of  Typhoid  Fever.     By  Wm.  W. 
;      Keen,  M.  D.,  LL.D.,  F,  R.  C.  S.  (Hon.),  Professor  of  the  Principles  of  Sur- 
gery and  of  Clinical  Surgery,  Jefferson  Medical  College,  Philadelphia,  etc. 
Octavo  volume  of  386  pages,  illustrated.     Cloth,  ^3.00  net. 

KEEN'S  OPERATION  BLANK.    Second  Edition,  Revised  Form. 

An  Operation  Blank,  with  Lists  of  Instruments,  etc.  Required  in  Various 
Operations.  Prepared  by  W.  W.  Keen,  M.  D.,  LL.D.,  F.  R.  C.S.  (Hon.), 
Professor  of  the  Principles  of  Surgery  and  of  Clinical  Surgery,  Jefferson 
Medical  College,  Philadelphia.     Price  per  pad,  of  50  blanks,  50  cts.  net. 


OF   W.   B.  SAUNDERS  &=    CO. 


KYLE  ON  THE  NOSE  AND  THROAT.    Second  Edition. 

Diseases  of  the  Nose  and  Throat.  By  D.  Braden  Kyle,  M.  D.,  Clinical 
Professor  of  Laryngology  and  Rhinology,  Jefferson  Medical  College,  Phila- 
delphia. Octavo,  646  pages  ;  over  150  illustrations  and  6  lithographic  plates. 
Cloth,  ^4.00  net ;  Sheep  or  Half  Morocco,  fc.oo  net. 

LAINE'S  TEMPERATURE  CHART. 

Temperature  Chart.  Prepared  by  D.  T.  LAiNfe,  M.  D.  Size  8  x  13^^ 
inches.  A  conveniently  arranged  Chart  for  recording  Temperature,  with 
columns  for  daily  amounts  of  Urinary  and  Fecal  Excretions,  Food,  Re- 
marks, etc.  On  the  back  of  each  chart  is  given  the  Brand  treatment  of 
Typhoid  Fever.     Price,  per  pad  of  25  charts,  50  cts.  net. 

LEVY,  KLEMPERER,  AND   ESHNER'S  CLINICAL  BACTERI= 
OLOQY. 

The  Elements  of  Clinical  Bacteriology.  By  Dr.  Ernst  Levy,  Professor 
in  the  University  of  Strasburg.  and  Dr.  Felix  Klemperer,  Privatdocent 
in  the  University  of  Strasburg.  Translated  and  edited  by  AUGUSTUS  A. 
EshNER,  M.  D.,  Professor  of  Clinical  Medicine,  Philadelphia  Polyclinic. 
Octavo,  440  pages,  fully  illustrated.     Cloth,  ^2.50  net. 

LOCKWOOD'S  PRACTICE  OF  MEDICINE. 

A  Manual  of  tlie  Practice  of  Medicine.  By  GEORGE  RoE  LOCKWOOD, 
M.  D.,  Professor  of  Practice  in  the  Women's  Medical  College  of  the  New 
York  Infirmary,  etc.      935  pages,  with  75  illustrations  in  the  text,  and  22 

full-page  plates.     Cloth,  $2.50  net. 

LONQ»S  SYLLABUS  OF  GYNECOLOGY. 

A  SvUabus  of  Gynecology,  arranged  in  Conformity  with  "An  American 
Text-Book  of  Gynecology."  By  J.  W.  LONG,  M.D.,  Professor  of  Dis- 
eases of  Women  and  Children,  Medical  College  of  Virginia,  etc.  Cloth, 
interleaved,  $1.00  net. 

MACDONALD'S  SURGICAL   DIAGNOSIS   AND  TREATMENT. 

Surgical  Diagnosis  and  Treatment.  By  J.  W,  MacdoNALD,  M.  D.  Edin., 
F.  R.  C.  S.  Edin.,  Professor  of  Practice  of  Surgery  and  Clinical  Surgery, 
Hamline  University.  Handsome  octavo,  800  pages,  fully  illustrated.  Cloth, 
$5.00  net;  Sheep  or  Half  Morocco,  ^6.00  net. 

MALLORY   AND   WRIGHT'S  PATHOLOGICAL  TECHNIQUE. 

Pathological  Technique.  A  Practical  Manual  for  Laboratory  Work  in 
Pathology,  Bacteriology,  and  Morbid  Anatomy,  with  chapters  on  Post- 
Mortem  Technique  and  the  Performance  of  Autopsies.  By  FRANK  B. 
Mallory,  A.m.,  M.  D.,  Assistant  Professor  of  Pathology,  Harvard  Uni- 
versity Medical  School,  Boston;  and  James  H.  Wright,  A.M.,  M.  D., 
Instructor  in  Pathology,  Harvard  University  Medical  School,  Boston.  Oc- 
tavo, 396  pages,  handsotnely   illustrated.     Cloth,  ^2.50  net. 

McFARLAND'S    PATHOGENIC    BACTERIA.      Third    Edition, 
increased  in  size  by  over  lOo  Pages. 

Text-Book  upon  the  Pathogenic  Bacteria.  By  JOSEPH  McFARLAND, 
M.D.,  Professor  of  Pathology  and  Bacteriology,  Medico-Chirurgical  Col- 
lege of  Philadelphia,  etc.  Octavo  volume  of  621  pages,  finely  illustrated. 
Cloth,  $3.25  net. 


MEDICAL   PUBLICATIONS 


MEIGS  ON  FEEDING  IN  INFANCY. 

Feeding  in  Early  Infancy.  By  Arthur  V.  Meigs,  M.  D.  Bound  in  limp 
cloth,  flush  edges,  25  cts.  net. 

MOORE'S  ORTHOPEDIC  SURGERY. 

A  Manual  of  Orthopedic  Surgery.  By  James  E.  Moore,  M,  D.,  Professor 
of  Orthopedics  and  Adjunct  Professor  of  Clinical  Surgery,  University  of 
Minnesota,  College  of  Medicine  ind  Surgery.  Octavo  volume  of  356  pages, 
handsomely  illustrated.     Cloth,  ^2.50  net. 

MORTEN'S  NURSES*  DICTIONARY. 

Nurses'  Dicdonary  of  Medical  Terms  and  Nursing  Treatment.  Containing 
Definitions  of  the  Principal  Medical  and  Nursing  Terms  and  Abbreviations; 
of  the  Instruments,  Drugs,  Diseases,  Accidents,  Treatments,  Operations, 
Foods,  Appliances,  etc.  encountered  in  the  ward  or  in  the  sick-room.  By 
HONNOR  Morten,  author  of"  How  to  Become  a  Nurse,"  etc.  i6mo,  140 
pages.     Cloth,  ^i.oo  net. 

NANCREDE'S  ANATOMY  AND  DISSECTION.    Fourth  Edition. 

Essentials  of  Anatomy  and  Manual  of  Practical  Dissection.  By  CHARLES 
B.  Nancrede,  M.  D.,  LL.D.,  Professor  of  Surgery  and  of  Clinical  Surgery, 
University  of  Michigan,  Ann  Arbor.  Post-octavo,  500  pages,  with  full-page 
lithographic  plates  in  colors  and  nearly  200  illustrations.  Extra  Cloth  (or 
Oilcloth  for  dissection-room),  $2.00  net. 

NANCREDE'S  PRINCIPLES  OF  SURGERY. 

Lectures  on  the  Principles  of  Surgery.  By  CHARLES  B.  NANCREDE,  M.  D., 
LL.D,,  Professor  of  Surgery  and  of  Clinical  Surgery,  University  of  Michigan, 
Ann  Arbor.     Octavo,  398  pages,  illustrated.     Cloth,  ^2.50  net. 

NORRIS'S    SYLLABUS    OF    OBSTETRICS.     Third    Edition, 
Revised. 

Syllabus  of  Obstetrical  Lectures  in  the  Medical  Department  of  the  University 
of  Pennsylvania.  By  RICHARD  C.  NORRIS,  A.  M.,  M,  D.,  Instructor  in 
Obstetrics  and  Lecturer  on  Clinical  and  Operative  Obstetrics,  University 
of  Pennsylvania.  Crown  octavo,  222  pages.  Cloth,  interleaved  for  notes, 
52.00  net. 

OGDEN  ON  THE  URINE. 

Clinical  Examination  of  the  Urine  and  Urinary  Diagnosis.  A  Clinical  Guide 
for  the  Use  of  Practitioners  and  Students  of  Medicine  and  Surgery.  By  J. 
Bergen  Ogden,  M.  D.,  Instructor  in  Chemistry,  Harvard  University  Med- 
ical School.  Handsome  octavo,  416  pages,  with  54  illustrations,  and  a  num- 
ber of  colored  plates.     Cloth,  ^3.00  net. 

PENROSE»S  DISEASES  OF  WOMEN.    Third  Edition,  Revised. 

A  Text-Book  of  Diseases  of  Women.  By  Charles  B.  Penrose,  M.  D., 
Ph.  D.,  formerly  Professor  of  Gynecology  in  the  University  of  Pennsylvania. 
Octavo  volume  of  531  pages,  handsomely  illustrated.     Cloth,  $3.75  net. 


OF  W.  B.   SAUNDERS  &>  CO. 


PRYOR— PELVIC  INFLAMMATIONS. 

The  Treatment  of  Pelvic  Inflammations  through  the  Vagina.  By  W.  R. 
Pryor,  M.  D.,  Professor  of  Gynecology,  New  York  Polyclinic.  i2mo,  248 
pages,  handsomely  illustrated.     Cloth,  ^2.00  net. 

PYE'S  BANDAGING. 

Elementary  Bandaging  and  Surgical  Dressing.  With  Directions  concerning 
the  Immed  ate  Treatment  of  Cases  of  Emergency.  By  WALTER  Pye, 
F.  R.  C.  S.,  late  Surgeon  to  St.  Mary's  Hospital,  London.  Small  i2mo, 
over  80  illustrations.     Cloth,  flexible  covers,  75  cts.  net. 

PYLE'S  PERSONAL  HYGIENE. 

A  Manual  of  Personal  Hygiene.  Proper  Living  upon  a  Physiologic  Basis. 
Edited  by  WALTER  L.  Pyle,  M.  Dt,  Assistant  Surgeon  to  the  Wills  Eye 
Hospital,  Philadelphia.  Octavo  volume  of  344  pages,  fully  illustrated. 
Cloth,  ^1.50  net. 

RAYMOND'S  PHYSIOLOGY. 

A  Manual  of  Physiology.  By  Joseph  H.  Raymond,  A.  M„  M.  D.,  Pro- 
fessor of  Physiology  and  Hygiene  and  Lecturer  on  Gynecology  in  the  Long 
Island  College  Hospital.  382  pages,  102  illustrations,  and  4  full-page  colored 
plates.     Cloth,  $1.25  net. 

SALINGER  AND  KALTEYER'S  MODERN  MEDICINE. 

Modern  Medicine.  By  JULIUS  L.  Salinger,  M.  D.,  Demonstrator  of 
Clinical  Medicine,  Jefferson  Medical  College  ;  and  F.  J.  Kalteyer,  M.  D., 
Assistant  Demonstrator  of  Clinical  Medicine,  Jefferson  Medical  College. 
Handsome  octavo,  801  pages,  illustrated.     Cloth,  ^4.00  net. 

SAUNDBY'S  RENAL  AND  URINARY  DISEASES. 

Lectures  on  Renal  and  Urinary  Diseases.  By  Robert  Saundby,  M.  D. 
Edin.,  Fellow  of  the  Royal  College  of  Physicians,  London,  and  of  the  Royal 
Medico-Chirurgical  Society ;  Professor  of  Medicine  in  Mason  College,  Bir- 
mingham, etc.  Octavo,  434  pages,  with  numerous  illustrations  and  4  colored 
plates.     Cloth,  $2.50  net. 

SAUNDERS'  MEDICAL  HAND=ATLASES.    See  pp.  16  and  17. 

SAUNDERS'   POCKET   MEDICAL   FORMULARY.     Sixth   Edi- 
tion, Revised. 

By  William  M.  Powell,  M.  D.,  author  of  "  Essentials  of  Diseases  of 
Children"  ;  Member  of  Philadelphia  Pathological  Society.  Containing  1844 
formulae  from  the  best-known  authorities.  With  an  Appendix  containing 
Posological  Table,  Formulae  and  Doses  for  Hypodermic  Medication. 
Poisons  and  their  Antidotes,  Diameters  of  the  Female  Pelvis  and  Fetal 
Head,  Obstetrical  Table,  Diet  List  for  Various  Diseases,  Materials  and 
Drugs  used  in  Antiseptic  Surgery,  Treatment  of  Asphyxia  from  Drowning, 
Surgical  Remembrancer,  Tables  of  Incompatibles,  Eruptive  Fevers,  etc., 
etc.  Handsomely  bound  in  flexible  morocco,  with  side  index,  wallet,  and 
flap.     $2.00  net. 

SAUNDERS'  QUESTION=COMPENDS.     See  pages  14  and  15. 


12  MEDICAL   PUBLICATIONS 


SCUDDER'S  FRACTURES.     Second  Edition,  Revised. 

The  Treatment  of  Fractures.  By  Chas  L.  Scudder,  M.D.,  Assistant  in 
Clinical  and  Operative  Surgery,  Harvard  University  Medical  School.  Oc- 
tavo, 433  pages,  with  nearly  600  original  illustrations.  Polished  Buckram, 
^^4.50  net ;   Half  Morocco,  ^5.50  net. 

SENN'S  QENITO=URINARY  TUBERCULOSIS. 

Tuberculosis  of  the  Genito-Urinary  Organs,  Male  and  Female.  By  NICH- 
OLAS Senn,  M.  D.,  Ph.  D.,  LL.D.,  Professor  of  the  Practice  of  Surgery  and 
of  Clinical  Slirgery,  Rush  Medical  College,  Chicago.  Handsome  octavo 
volume  of  320  pages,  illustrated.     Cloth,  ^3.00  net. 

SENN'S  PRACTICAL  SURGERY. 

Practical  Surgery.  By  Nicholas"  Senn,  M.  D.,  Ph.D.,  LL.D.,  Professor 
of  the  Practice  of  Surgery  and  of  Clinical  Surgery,  Rush  Medical  College, 
Chicago.  Handsome  octavo  volume  of  over  1000  pages,  profusely  illus- 
trated.    In  Press. 

SENN'S  SYLLABUS  OF  SURGERY. 

A  Syllabus  of  Lectures  on  the  Practice  of  Surgery,  arranged  in  conformity 
with  "  An  American  Text-Book  of  Surgery."  By  NICHOLAS  SENN,  M.  D., 
Ph.D.,  LL.D.,  Professor  of  the  Practice  of  Surgery  and  of  Clinical  Surgery. 
Rush  Medical  College,  Chicago.     Cloth,  ^1.50  net. 

SENN'S  TUMORS.    Second  Edition,  Revised. 

Pathology  and  Surgical  Treatment  of  Tumors.  By  NICHOLAS  SENN,  M.  D., 
Ph.D.,  LL.D.,  Professor  of  the  Practice  of  Surgery  and  of  Clinical  Surgery, 
Rush  Medical  College,  Chicago.  Octavo  volume  of  718  pages,  with  478 
illustrations,  includidg  12  full-page  plates  in  colors.  Cloth,  ^5.00  net ;  Sheep 
or  Half  Morocco,  ^6.00  net. 

STARR'S  DIETS  FOR  INFANTS  AND  CHILDREN. 

Diets  for  Infants  and  Children  in  Health  and  in  Disease.  By  LOUIS  STARR, 
M.  D.,  Editor  of  "An  American  Text-Book  of  the  Diseases  of  Children." 
230  blanks  (pocket-book  size),  perforated  and  neatly  bound  in  flexible 
morocco.     $1.25  net. 

STENGEL'S  PATHOLOGY.  Third  Edition,  Thoroughly  Revised. 

A  Text-Book  of  Pathology.  By  ALFRED  Stengel.  M.  D.,  Professor  of 
Clinical  Medicine,  University  of  Pennsylvania ;  Visiting  Physician  to  the 
Pennsylvania  Hospital.  Handsome  octavo,  873  pages,  nearly  400  illustra- 
tions, many  of  them  in  colors.  Cloth,  $5.00  net;  Sheep  or  Half  Morocco, 
^6.00  net. 

STENGEL  AND  WHITE  ON  THE  BLOOD. 

The  Blood  in  its  Clinical  and  Pathological  Relations.  By  Alfred  Sten- 
gel. M.  D.,  Professor  of  Clinical  Medicine,  University  of  Pennsylvania;  and 
C.Y.White,  Jr.,  M.D.,  Instructor  in  Clinical  Medicine,  University  of 
Pennsylvania.     In  Press. 


OF   W.  B.  SAUNDERS  &-   CO.  13 


STEVENS'  MATERIA  MEDICA  AND  THERAPEUTICS.    Sec- 
ond Edition,  Revised. 

A  Manual  of  Materia  Medica  and  Therapeutics.  By  A.  A.  Stevens,  A.  M., 
M.  D.,  Lecturer  on  Physical  Diagnosis  in  the  University  of  Pennsylvania. 
Post-octavo,  445  pages.     Flexible  Leather,  ^2.00  net. 

STEVENS'  PRACTICE  OF  MEDICINE.     Fifth  Edition,  Revised. 

A  Manual  of  the  Practice  of  Medicine.  By  A.  A.  STEVENS,  A.  M.,  M.  D., 
Lecturer  on  Physical  Diagnosis  in  the  University  of  Pennsylvania.  Spe- 
cially intended  for  students  preparing  for  graduation  and  hospital  examina- 
tions.    Post-octavo,  519  pages  ;  illustrated.     Flexible  Leather,  $2.00  net. 

STEWART'S  PHYSIOLOGY.     Fourth  Edition,  Revised. 

A  Manual  of  Physiology,  with  Practical  Exercises.  For  Students  and  Prac- 
titioners. By  G.  N.  Stewart,  M.  A.,  M.  D.,  D.  Sc.  Professor  of  Physiol- 
ogy in  the  Western  Reserve  University,  Cleveland,  Ohio.  Octavo  volume 
of  894  pages  ;  336  illustrations  and  5  colored  plates.     Cloth,  $3.75  net. 

STONEY'S  MATERIA  MEDICA  FOR  NURSES. 

Materia  Medica  for  Nurses.  By  EMILY  A.  M.  Stoney,  late  Superintend- 
ent of  the  Training-School  for  Nurses,  Carney  Hospital,  South  Boston, 
Mass.     Handsome  octavo  volume  of  306  pages.     Cloth,  $1.50  net. 

STONEY'S  NURSING.    Second  Edition,  Revised. 

Practical  Points  in  NuBsing.  For  Nurses  in  Private  Practice.  By  EMILY 
\.  M.  Stoney,  late  Superintendent  of  the  Training-School  for  Nurses, 
Carney  Hospital,  South  Boston,  Mass.  456  pages,  with  73  engravings  and 
8  colored  and  half-tone  plates.     Cloth,  ^1.75  net. 

STONEY'S  SURGICAL  TECHNIC  FOR  NURSES. 

Bacteriology  and  Surgical  Technic  for  Nurses.  By  EMILY  A.  M.  STONEY, 
late  Superintendent  of  the  Training-School  for  Nurses,  Carney  Hospital, 
South  Boston,  Mass.     i2mo  volume,  fully  illustrated.     Cloth,  ^1.25  net. 

THOMAS'S  DIET  LISTS.     Second  Edition,  Revised. 

Diet  Lists  and  Sick-Room  Dietary.  By  JEROME  B.  THOMAS,  M.  D.,  In- 
structor in  Materia  Medica,  Long  Island  Hospital ;  Assistant  Bacteriologist 
to  the  Hoagland  Laboratory.     Cloth,  ^1.25  net.     Send  for  sample  sheet. 

THORNTON'S  DOSE-BOOK  AND  PRESCRIPTION=VV^RITING. 

Dose-Book  and  Manual  of  Prescription-Writing.  By  E.  Q.  THORNTON, 
M.  D.,  Demonstrator  of  Therapeutics,  Jefferson  Medical  College,  Philadel- 
phia.    334  pages,  illustrated.     Cloth,  $1.25  net. 

VAN  VALZAH  AND  NISBET'S  DISEASES  OF  THE  STOMACH. 

Diseases  of  the  Stomach.  By  WILLIAM  W.  Van  Valzah,  M.  D.,  Pro- 
fessor of  General  Medicine  and  Diseases  of  the  Digestive  System  and  the 
Blood,  New  York  Polyclinic;  and  J.  Douglas  Nisbet,  M.  D.,  Adjunct 
Professor  of  General  Medicine  and  Diseases  of  the  Digestive.  System  and 
the  Blood,  New  York  Polyclinic.  Octavo  volume  of  674  pages,  illustrated. 
Cloth.  $3.50  net. 


14  MEDICAL   PUBLICATIONS. 


VECKrS  SEXUAL  IMPOTENCE. 

The  Pathology  and  Treatment  of  Sexual  Impotence.  By  VICTOR  G.  Vecki, 
M.  D.  From  the  second  German  edition,  revised  and  enlarged.  Demi- 
octavo,  291  pages.     Cloth,  ^2.00  net. 

VIERORDT'S    MEDICAL    DIAGNOSIS.      Fourth    Edition,   Re= 
vised. 

Medical  Diagnosis.  By  Dr.  Oswald  Vierordt,  Professor  of  Medicine, 
University  of  Heidelberg.  Translated,  with  additions,  from  the  fifth  en- 
larged German  edition,  with  the  author's  permission,  by  Francis  H. 
Stuart,  A.  M.,  M.  D.  Handsome  octavo  volume,  603  pages;  194  wood- 
cuts, many  of  them  in  colors.  Cloth,  4.00  net;  Sheep  or  Half-Morocco, 
JJ55.00  net. 

WATSON'S  HANDBOOK  FOR  NURSES. 

A  Handbook  for  Nurses.  By  J.  K.  Watson,  M.  D.  Edin.  American 
Edition,  under  supervision  of  A.  A.  Stevens,  A.  M.,  M.  D.,  Lecturer  on 
Physical  Diagnosis,  University  of  Pennsylvania.  i2mo,  413  pages,  73  illus- 
trations.    Cloth,  ^1.50  net. 

WARREN'S  SURGICAL  PATHOLOGY.    Second  Edition. 

Surgical  Pathology  and  Therapeutics.  By  JOHN  COLLINS  Warren,  M.  D., 
LL.D.,  F.  R.  C.  S.  (Hon.),  Professor  of  .Surgery,  Harvard  Medical  School. 
Handsome  octavo,  873  pages  ;  136  relief  and  lithographic  illustrations,  33  in 
colors.  With  an  Appendix  on  Scientific  Aids  to  Surgical  Diagnosis,  and  a 
series  of  articles  on  Regional  Bacteriology.  Cloth  ^5.00  net ;  Sheep  or 
Half  Morocco.  S6.00  net. 


SAUNDERS' 
QUEST  ION  =  COMPENDS, 


ARRANGED  IN  QUESTION  AND  ANSWER  FORM. 


The  Most  Complete  and  Best  Illustrated  Series  of  Compends  Ever  Issued. 


NOW  THE  STANDARD  AUTHORITIES  IN  MEDICAL  LITERATURE 

W^ITH 

Students  and  Practitioners  in  every  City  of  the  United  States  and  Canada. 


Since  the  issue  of  the  first  volume  of  the  Saunders  Question-Compends, 

OVER  175,000  COPIES 

of   these   unrivalled   publications    have   been    sold.      This   enormous   sale   is   indisputable 
evidence  of  the  value  of  these  self-helps  to  students  and  physicians. 

SEE  NEXT  PAGE  FOR  LIST. 


Saunders' 
Question=Compend    Series 

Price,  Cloth,  $i.oo  net  per  copy,  except  when  otherwise  noted. 


Where  the  work  ot  preparing  students'  manuals  is  to  end  we  cannot  say,  but  the  Saunders 
Series,  in  our  opinion,  bears  off  the  palm  at  present." — New  York  Medical  Record. 


1.  Essentials  of  Physiology.     A  new  work  in  preparation. 

2.  Essentials  of  Surgery.     By  Edward  Martin,  M.  D.     Seventh  edition,  revised, 

with  an  Appendix  and  a  chapter  on  Appendicitis. 

3.  Essentials  of  Anatomy.     By  Charles   B.   Nancrede,   M.  D.     Sixth   edition. 

thoroughly  revised  and  enlarged. 

4.  Essentials  of  Medical  Chemistry,  Organic  and  Inorganic.    By  Lawrence 

Wolff,  M.  D.     Fifth  edition,  revised. 

5.  Essentials  of  Obstetrics.     By  W.  Easterly  Ashton,  M.  D.     Fourth   edition, 

revised  and  enlarged. 

6.  Essentials  of  Pathology  and  Morbid  Anatomy.    By  F.  j.  Kalteyer,  m.  d. 

In  preparation. 

7 .  Essentials  of  Materia  Medica,  Therapeutics,  and  Prescription- Writing. 

By  Henry  Morris,  M.  D.     Fifth  edition,  revised. 

8.  9.     Essentials  of  Practice   of  Medicine.     By  Henry  Morris,  M.  D.     An  Ap- 

pendix on  Urine  Examination.  By  Lawrence  Wolff,  M.  D.  Third  edition, 
enlarged  by  some  300  Essential  Formulae,  selected  from  eminent  authorities,  by 
Wm.  M.  Powell,  M.  D.     (Double  number,  ;^i.5o  net.) 

10.  Essentials   of   Gynecology.     By   Edwin   B.  Cragin,  M.  D.      Fourth   edition, 

revised. 

11.  Essentials  of  Diseases  of  the  Skin.    By  Henry  w.  Stelwagon,  m.  d. 

Fourth  edition,  revised  and  enlarged. 

12.  Essentials  of  Minor  Surgery,  Bandaging,  and  Venereal  Diseases.    By 

Edward  Martin,  M.  D.     Second  edition,  revised  and  enlarged. 

13.  Essentials  of  Legal  Medicine,  Toxicology,  and  Hygiene.    This  volume  is 

at  present  out  of  print. 

14.  Essentials  of  Diseases  of  the  Eye,  Nose,  and  Throat.    By  Edward  Jack- 

son, M.  D.,  and  E.  B.  Gleasomj  M.  D.     Second  edition,  revised. 

15.  Essentials  of  Diseases  of  Children.     By  William  M.  Powell,  M.  D.     Second 

edition. 

16.  Essentials  of  Examination  of  Urine.     By  Lawrence  Wolff,  M.  D.     Colored 

"  Vogel  Scale."     (75  cents  net.) 

17.  Essentials  of  Diagnosis.    By  S.  Solis-Cohen,  m.  d.,  and  A.  A.  Eshner,  M.  D. 

Second  edition,  thoroughly  revised. 

18.  Essentials  of  Practice  of  Pharmacy.     By  Lucius  E.  Sayre.     Second  edition, 

revised  and  enlarged. 

20.  Essentials  of  Bacteriology.     By  M.  v.  Ball,  M.  D.     Fourth  edition,  revised. 

21.  Essentials  of  Nervous  Diseases  and  Insanity.    By  John  C.  Shaw,  M.  d. 

Third  edition,  revised. 

22.  Essentials  of  Medical  Physics.     By  Fred  J.  Brockway,  M.  D.     Second  edi- 

tion, revised. 

23.  Essentials  of  Medical  Electricity.     By  David  D.  Stewart,  M.  D.,  and   Ed- 

ward S.  Lawrance,  M.  D. 

24.  Essentials  of  Diseases  of  the  Ear.     By  E.  B.  Gleason,  M.  D.     Second  edition, 

revised  and  greatly  enlarged. 

A  NEW  VOLUME. 

25.  Essentials  of  Histology.    By  Louis  Leroy,  M.  D.     With  73  original  illustrations. 


Pamphlet  containing  specimen  pages,  etc.,  sent  free  upon  application. 

IS 


Saunders'  Medical  Hand=Atlases. 


VOLUMES  NOW  READY. 

ATLAS    AND    EPITOME    OF    INTERNAL    MEDICINE    AND 
CLINICAL   DIAGNOSIS. 

By  Dr.  Chr.  Jakob,  of  Erlangen.  Edited  by  Augustus  A.  Eshner, 
M.  D.,  Professor  of  Clinical  Medicine,  Philadelphia  Polyclinic,  With  179 
colored  figures  on  68  plates,  64  text-illustrations,  259  pages  of  text.  Cloth, 
^3.00  net. 

ATLAS  OF,  LEGAL  MEDICINE. 

By  Dr.  E.  R.  von  Hoffman,  of  Vienna.  Edited  by  Frederick  Peter- 
son, M.  D.,  Chief  of  Clinic,  Nervous  Department,  College  of  Physicians  and 
Surgeons,  New  York.  With  120  colored  figures  on  56  plates  and  193  beau- 
tiful half-tone  illustrations.     Cloth,  $3.50  net. 

ATLAS  AND  EPITOME  OF  DISEASES  OF  THE  LARYNX. 

By  Dr.  L,  Grunwald,  of  Munich.  Edited  by  CHARLES  P.  Grayson, 
M.  D.,  Physician-in-Charge,  Throat  and  Nose  Department,  Hospital  of  the 
University  of  Pennsylvania.  With  107  colored  figures  on  44  plates,  25  text- 
illustrations,  and  103  pages  of  text.     Cloth,  ^2.50  net. 

ATLAS  AND  EPITOME  OF  OPERATIVE  SURGERY. 

By  Dr.  O,  Zuckerkandl,  of  Vienna.  Edited  by  J.  Chalmers  DaCosta, 
M.D.,  Professor  of  Principles  of  Surgery  and  Clinical  Surgery,  Jefferson 
Medical  College,  Philadelphia.  With  24  colored  plates,  214  text-illustra- 
tions, and  395  pages  of  text.     Cloth,  ^3.00  net. 

ATLAS  AND  EPITOME  OF  SYPHILIS  AND  THE  VENEREAL 

DISEASES. 

By  Prof.  Dr.  Franz  Mracek,  of  Vienna.  Edited  by  L.  Bolton  Bangs, 
M.  D.,  Professor  of  Genito-Urinary  Surgery,  University  and  Bellevue  Hos- 
pital Medical  College,  New  York.  With  71  colored  plates,  16  illustrations, 
and  122  pages  of  text.     Cloth,  ^3.50  Tiet. 

ATLAS  AND  EPITOME  OF  EXTERNAL  DISEASES  OF  THE 
EYE. 

By  Dr.  O.  Haab,  of  Zurich,  Edited  by  G.  E.  de  Schweinitz,  M.  D., 
Professor  of  Ophthalmology,  Jefferson  Medical  College,  Philadelphia.  With 
76  colored  illustrations  on  40  plates  and  228  pages  of  text.     Cloth,  ^3.00  net, 

ATLAS  AND  EPITOME  OF  SKIN  DISEASES. 

By  Prof.  Dr.  Franz  Mracek,  of  Vienna.  Edited  by  Henry  W,  Stel- 
WAGON.  M.  D.,  Clinical  Professor  of  Dermatology,  Jefferson  Medical  Col- 
lege, Philadelphia.  With  63  colored  plates,  39  half-tone  illustrations,  and 
.200  pages  of  text.     Cloth,  ^3.50  net. 

ATLAS  AND  EPITOME  OF  SPECIAL  PATHOLOGICAL  HIS- 
TOLOGY. 

By  Dr.  H.  Durck,  of  Munich.  Edited  by  LUDWIG  Hektoen,  M.  D., 
Professor  of  Pathology,  Rush  Medical  College,  Chicago.  In  Two  Parts. 
Part  I.  Ready\  including  Circulatory,  Respiratory,  and  Gastro-intestinal 
Tract,  120  colored  figures  on  62  plates,  158  pages  of  text.  Part  H,  Ready 
Shortly.     Price  of  Part  I,,  ^3,00  net, 

16 


Saunders'  Medical  Iiand= Atlases. 


VOLUMES  JUST  ISSUED. 

ATLAS  AND  EPITOME   OF   DISEASES  CAUSED  BY  ACCI- 
DENTS. 

By  Dr.  Ed.  Golebiewski,  of  Berlin.  Translated  and  edited  with  addi- 
tions by  Pearce  Bailey,  M.  D.,  Attending  Physician  to  the  Department 
of  Corrections  and  to  the  Almshouse  and  Incurable  Hospitals,  New  York. 
With  40  colored  plates,  143  text-illustrations,  and  600  pages  of  text.  Cloth, 
$4.00  net. 

ATLAS  AND  EPITOME  OF  GYNECOLOGY. 

By  Dr.  O.  Shaeffer,  of  Heidelberg.  From  the  Second  Revised  German 
Edition.  Edited  by  RICHARD  C.  NORRIS,  A.  M.,  M.D..  Gynecologist  to 
the  Methodist  Episcopal  and  the  Philadelphia  Hospitals  ;  Surgeon-in-Charge 
of  Preston  Retreat,  Philadelphia.  With  90  colored  plates,  65  text-illustra- 
tions, and  308  pages  of  text.     Cloth,  $3.50  net. 

ATLAS   AND   EPITOME  OF  THE  NERVOUS  SYSTEM  AND 

ITS  DISEASES. 

By  Professor  Dr.  Chr.  Jakob,  of  Erlangen.  From  the  Second  Revised 
German  Edition.  Edited 'by  EDWARD  D.  FiSHER,  M.  D.,  Professor  of 
Diseases  of  the  Nervous  System,  University  and  Belle vue  Hospital  Medical 
College,  New  York.    With  83  plates  and  a  copious  text.    ^3.50  net. 

ATLAS   AND   EPITOME  OF  LABOR  AND  OPERATIVE  OB- 
STETRICS. 

By  Dr.  O.  Shaeffer,  of  Heidelberg,  From  the  Fifth  Revised  German 
Edition.  Edited  by  J.  Clifton  Edgar,  M.  D.,  Professor  of  Obstetrics  and 
Clinical  Midwifery,  Cornell  University  Medical  School.  With  126  colored 
illustrations,     $2,00  net. 

ATLAS  AND  EPITOME  OF  OBSTETRICAL  DIAGNOSIS  AND 
TREATMENT. 

By  Dr.  O.  Shaeffer,  of  Heidelberg.  From  the  Second  Revised  German 
Edition.  Edited  by  J.  CLIFTON  Edgar,  M.  D,,  Professor  of  Obstetrics 
and  Clinical  Midwifery,  Cornell  University  Medical  School.  72  colored 
plates,  numerous  te.xt-illustrations,  and  copious  text.     ^3.00  net. 


IN   PRESS  FOR  EARLY  PUBLICATION. 

ATLAS  AND   EPITOME  OF  OPHTHALMOSCOPY  AND  OPH- 
THALMOSCOPIC  DIAGNOSIS. 

By  Dr.  O.  Haab,  of  Zurich.  From  the  Third  Revised  and  Enlarged  Ger- 
man Edition.  Edited  by  G.  E.  DE  SCHWEINITZ,  M.  D.,  Professor  of  Oph- 
thalmology. Jefferson  Medical  College,  Philadelphia.  With  149  colored 
figures  and  82  pages  of  text. 


ADDITIONAL  VOLUMES   IN  PREPARATION. 

17 


CLASSIFIED  LIST 

OF  THE 

MEDICAL    PUBLICATIONS 

OF 

W.  B.  SAUNDERS  &  COMPANY 


ANATOMY,  EMBRYOLOGY.  HIS- 
TOLOGY. 

Bohm,  Davidoff,  and  Huber— A  Text- 
Book  of  Histolo^, 4 

Clarkson — A  Text-Book  of  Histology,  .  5 
Haynes — A  Manual  of  Anatomy,  ...  7 
Heisler — A  Text-Book  of  Embryology,  .  7 
Leroy — Essentials  of  Histology,  ....  15 
Nancrede — Essentials  of  Anatomy,  ...  15 
Nancrede — Essentials  of  Anatomy  and 
Manual  of  Practical  Dissection,  ....    10 

BACTERIOLOGY.     * 

Ball — Essentials  of  Bacteriology,  ....  15 

Crookshank — Bacteriology, 5 

Frothingham — Laboratory  Guide,  ...  6 
Levy  and  Klemperer's  Clinical  Bacte- 
riology,      9 

Mallory    and     Wright  —  Pathological 

Technique, 9 

McFarland— Pathogenic  Bacteria,  ...  9 

CHARTS,  DIET-LISTS.  ETC. 

Griffith — Infant's  Weight  Chart,  ....  7 
Hart— Diet  in  Sickness  and  in  Health,    .     7 

Keen— Operation  Blank,      8 

Laine — Temperature  Chart, 9 

Meigs — Feeding  in  Early  Infancy,  ...  10 
Starr — Diets  for  Infants  and  Children,  .  12 
Thomas— Diet-Lists, 13 

CHEMISTRY  AND  PHYSICS. 
Brockway  —  Essentials   of   Medical 

Physics, 15 

Wolff"— Essentials  of  Medical  Chemistry,   15 

CHILDREN. 
An  American  Text-Book  of  Diseases 

of  Children 1 

Griffith— Care  of  the  Baby, 7 

Griffith— Infant's  Weight  Chart,  ....      7 
Meigs — Feeding  in  Early  Infancy,       .    .    10 
Powell— Essentials  of  Diseases  of  Chil- 
dren,      15 

Starr — Diets  for  Infants  and  Children,    .   12 

DIAGNOSIS. 

Cohen  and  Eshner— Essentials  of  Diag- 
nosis,     15 

C  irwin- Physical  Diagnosis, 5 

Macdonald — Surgical     Diagnosis     and 


Treatment, 


Vierordt —Medical  Diagnosis, 14 

DICTIONARIES. 

The  American  Illustrated  Medical 
Dictionary,     .    .  3. 

The  American  Pocket  Medical  Dic- 
tionary,     3 

Morton — Nurses'  Dictionary,   .   ,   .   .    ,   10 


I  EYE,  EAR,  NOSE,  AND  THROAT. 

I  An  American  Text-Book  of  Diseases 
j      of  the  Eye,  Ear,  Nose,  and  Throat,  .    .      i 
De  Schweinitz— Diseases  of  the  Eye,   .     6 
j  Friedrich  and  Curtis— Rhinology,  Lar- 

I      yngology,  and  Otology, 6 

[  Gleason — Essentials  of  Diseases  of  the 

Ear, 15 

I  Grunwald  and  Grayson— Atlas  of  Dis- 

i      eases  of  the  Larynx, 16 

I  H  dab  and  DeSchweinitz— Atlas  of  Ex- 
ternal Diseases  of  the  Eye, 16 

!  Jackson— Manual  of  Diseases  of  the  Eye,     8 
I  Jackson    and    Gleason— Essentials    of 
Diseases  of  the  Eye,  Nose,  and  Throat,   15 
Kyle— Diseases  of  the  Nose  and  Throat,     9 

I  GENITO-URINARY. 

j  An   American   Text-Book   of  Genito- 
urinary and  Skin  Diseases, 2 

Hyde  and  Montgomery— Syphilis  and 

the  Venereal  Diseases,       .   ', 8 

Martin— Essentials   of    Minor   Surgery," 

Bandaging,  and  Venereal  Diseases,  .  .  15 
Mracek  and   Bangs— Atlas  of  Syphilis 

and  the  Venereal  Diseases, 16 

Saundby— Renal  and  Urinary  Diseases,  11 
Senn—Genito- Urinary  Tuberculosis,  .  .  la 
Vecki — Sexual  Impotence, 14 

j        GYNECOLOGY. 

American  Text-Book  of  Gynecology,   .  a 

Cragin — Essentials  of  Gynecology,      .    .  15 

Garrigues— Diseases  of  Women,  ....  6 

Long — Syllabus  of  Gynecology,    ....  9 

Penrose — Diseases  of  Women, lo 

j  Pryor — Pelvic  Inflammations, 11 

Schaeff'er  and  Norris— Atlas  of  Gyne- 
cology,       17 

MATERIA  MEDICA,  PHARMA- 
COLOGY,  AND  THERAPEUTICS. 

An  American  Text-Book  of  Applied 

Therapeutics, i 

Butler— Text-Book  of  Materia  Medica, 

Therapeutics,  and  Pharmacology,  .  .  4 
Cerna— Notes  on  the  Newer  Remedies,  .  4 
Morris— Essentials  of   Materia   Medica 

and  Therapeutics 15 

Saunders'  Pocket  Medical  Formulary,  .  n 
Sayre — Essentials  of  Pharmacy,  ....  15 
Stevens— Manual  of  Therapeutics,  ...  13 
Stoney — Materia  Medica  for  Nurses,  .  .  13 
Thornton— Dose-Book  and   Manual  of 

Prescription- Writing,      13 

MEDICAL  JURISPRUDENCE  AND 
TOXICOLOGY. 

Chapman— Medical  Jurisprudence  and 
Toxicology, 5 


MEDICAL  PUBLICATIONS 


19 


Golebiewski  and  Bailey— Atlas  of  Dis-  ' 
eases  Caused  by  Accidents, 17 

Hofmann  and  Peterson— Atlas  of  Legal  \ 
Medicine, 16  j 

NERVOUS    AND    MENTAL    DIS-  ' 

EASES.  ETC. 
Chapin — Compendium  of  Insanity,  ...      5 
Church   and    Peterson— Nervous   and 

Mental  Diseases, 5 

Shaw — Essentials  of  Nervous  Diseases 

and  Insanity, 15 

NURSING. 
Davis — Obstetric  and  Gynecologic  Nurs- 
ing,     6 

Griffith— The  Care  of  the  Baby,  ....  7 

Hart — Diet  in  Sickness  and  in  Health,  .    .  7 

Meigs — Feeding  in  Early  Infancy,    ...  10 

Morten — Nurses'  Dictionary 10 

Stoney— Materia  Medica  for  Nurses,  .    .  13 

btoney — Practical  Points  in  Nursing,  .    .  13 

Sconey — Surgical  Technic  for  Nurses,    .  13 

Watson— Handbook  for  Nurses,  ....  14 


OBSTETRICS. 

An  American  Text-Book  of  Obstetrics 
Ashton — Essentials  of  Obstetrics,  .  .  . 
Boisliniere — Obstetric  Accidents,  .  . 
Dorland— Manual  of  Obstetrics,  .  .  . 
Hirst— Text-Book  of  Obstetrics,  .  .  . 
Norris — Syllabus  of  Obstetrics,  .  .  .  . 
SchaefFer  and  Edgar— Atlas  of  Obstet 
rical  Diagnosis  and  Treatment,  .    .    . 


17 


PATHOLOGY. 
An  American  Text-Book  of  Pathology.     2 
Durck  and  Hektoen— Atlas  of  Patho- 
logic Histology, 16 

Kalteyer — Essentials  of  Pathology,   .   .    15 
Mallory    and    Wright  — Pathological 

Technique, 9 

Senn — Pathology,  and  Surgical  Treat- 
ment of  Tumors, 12 

Stengel— Text-Book  of  Pathologry,  ...    12 
W^arren— Surgical  Pathology,   ....       14 

PHYSIOLOGY. 

An  American  Text-Book  of  Physiol- 

<3gy, 2 

— Essentials  of  Physiology, 15 

Raymond -Manual  of  Physiology,     .   .   11 
Stewart— Manual  of  Physiology,   ...   13 

PRACTICE  OF  MEDICINE. 

An  American  Year-Book  of  Medicine 
and  Surgery, 3 

Anders— Text-Book  of  the  Practice  of 
Medicine, 4 

Eichhorst — Practice  of  Medicine,  ...     6 

Lockwood — Practice  of  Medicine,  ...     9 

Morris — Essentials  of  Practice  of  Medi- 
cine, .       15 

Salinger  and  Kalteyer— Modern  Medi- 
cine,     "i-^ 

Stevens—Manual  of  Practice  of  Medi- 
cine,   13 


SKIN  AND  VENEREAL. 

An  American  Text-Book  of  Genito- 
urinary and  Skin  Diseases, 1 

Hyde  and  Montgomery— Syphilis  and 
the  Venereal  Diseases, 8 

Martin — Essentials  of  Minor  Surgery, 
Bandaging,  and  Venereal  Diseases,  .    .    15 

Mracek  and  Stelwagon — Atlas  of  Dis- 
eases of  the  Skin, 16 

Stelwagon— Essentials  of  Diseases  of 
the  Skin, 15 

SURGERY. 

An  American  Text-Book  of  Surgery,  2 
An  American  Year-Book  of  Medicine 

and  Surgery, 3 

Beck — Fractures, 4 

Beck— Manual  of  Surgical  Asepsis,  ...  4 

Da  Costa — Manual  of  Surgery, 5 

International  Text-Book  of  Surgery,  .  8 

Keen— Operation  Blank, 8 

Keen— The  Surgical  Complications  and 

Sequels  of  Typhoid  Fever, 8 

Macdonald  —  Surgical     Diagnosis    and 

Treatment, 9 

Martin — Essentials  of    Minor    Surgery, 

Bandaging,  and  Venereal  Diseases,  .    .  15 

Martin— Essentials  of  Surgery, 15 

Moore— Orthopedic  Surgery, 10 

Nancrede— Principles  of  Surgery,  .    .    .  10 

Pye— Bandaging  and  Surgical  Dressing,  ii 

Scudder — Treatment  of  Fractures,   ...  12 

Senn— Genito-Urinary  Tuberculosis,   .    .  12 

Senn— Practical  Surgery, 12 

Senn— Syllabus  of  Surgery,   ......  12 

Senn — Pathology  and  Surgical  Treat- 
ment of  Tumors, ...  12 

Warren— Surgical  Pathology  and  Ther- 
apeutics,    14 

Zuckerkandl  and  Da  Costa— Atlas  of 

Operative  Surgery, 16 

URINE  AND  URINARY  DISEASES. 

Ogden — Clinical     Examination    of    the 

Urine, 10 

Saundby — Renal  and  Urinary  Diseases,   11 

Wolff— Examination  of  Urine, 15 

MISCELLANEOUS. 
Abbott — Hygiene  of  Transmissible  Dis- 
eases,       3 

Bastin — Laboratory  Exercises  in  Bot- 
any,          .    .     4 

Golebiewski  and  Bailey— Atlas  of  Dis- 
eases Caused  by  Accidents,  .       .        •    .    17 
Gould  and   Pyle — Anomalies  and  Curi- 
osities of  Medicine, 7 

Grafstrom— Massage, 7 

Keating— Examination  for  Life  Insur- 
ance,      8 

Pyle— A  Manual  of  Personal  Hygiene,  .  11 
Saunders'  Medical  Hand-Atlases,  .  16,  17 
Saunders'  Pocket  Medical  Formulary,  .  11 
Saunders'  Question-Compends,  .  .  14,  15 
Stewart  and  Lawrence — Essentials  of 

Medical  Electricity, 15 

Thornton— Dose-Book  and   Manual   of 

Prescription-Writing, 13 

Van  Valzah  and  Nisbet— Diseases  of 
the  Stomach, 13 


Nothnagei's  Encyclopedia 


OF 


Special  Pathology  and  Therapeutics. 


IT  is  universally  acknowledged  that  the  Germans  lead  the  world  in  Internal  Medicine; 
*  and  of  all  the  German  works  on  this  subject.  Nothnagel's  "Special  Pathology  and 
Therapeutics"  is  conceded  by  scholars  to  be  without  question  the  best  System  of 
Medicine  in  existence.  So  necessary  is  this  book  in  the  study  of  Internal  Medicine 
that  it  comes  largely  to  this  country  in  the  original  German.  In  view  of  these  facts, 
Messrs.  W.  B.  Saunders  &  Company  have  arranged  with  the  publishers  to  issue  at  once 
an  authorized  edition  of  this  great  encyclopedia  of  medicine  in  English. 

For  the  present  a  set  of  some  ten  or  twelve  volumes,  representing  the  most  practical 
part  of  this  encyclopedia,  and  selected  by  a  competent  editor  with  especial  thought  of  the 
needs  of  the  practical  physician,  will  be  published.  These  volumes  will  contain  the 
real  essence  of  the  entire  work,  and  the  purchaser  will  therefore  obtain  at  less  than  half  the 
cost  the  cream  of  the  original.  Later  the  special  and  more  strictly  scientific  volumes  will 
be  offered  from  time  to  time. 

The  work  will  be  translated  by  men  possessing  thorough  knowledge  of  both  English  and 
German,  and  each  volume  will  be  edited  by  a  prominent  specialist  on  the  subject  to 
which  it  is  devoted.  It  will  thus  be  brought  thoroughly  up  to  date,  and  the  American  edition 
will  be  more  than  a  mere  translation  of  the  German ;  for,  in  addition  to  the  matter  contained 
in  the  original,  it  will  represent  the  very  latest  views  of  the  leading  American  special- 
ists in  the  various  departments  of  Internal  Medicine.  The  whole  System  will  be  under  the 
editorial  supervision  of  a  clinician  of  recognized  authority,  who  will  select  the  subjects 
for  the  American  edition,  and  will  choose  the  editors  of  the  different  volumes. 

Unlike  most  encyclopedias,  the  publication  of  this  work  will  not  be  extended  over  a 
number  of  years,  but  five  or  six  volumes  will  be  issued  during  the  coming  year,  and  the 
remainder  of  the  series  at  the  same  rate.  Moreover,  each  volume  will  be  revised  to  the 
date  of  its  publication  by  the  American  editor.  This  will  obviate  the  objection  that  has 
heretofore  existed  to  systems  published  in  a  number  of  volumes,  since  the  subscriber  will 
receive  the  completed  work  while  the  earlier  volumes  are  still  fresh. 

The  usual  method  of  publishers,  when  issuing  a  work  of  this  kind,  has  been  to  compel 
physicians  to  take  the  entire  System.  This  seems  to  us  in  many  cases  to  be  undesirable. 
Therefore,  in  purchasing  this  encyclopedia,  physicians  will  be  given  the  opportunity  of 
subscribing  for  the  entire  System  at  one  time ;  but  any  single  volume  or  any  number  of 
volumes  may  be  obtained  by  those  who  do  not  desire  the  complete  series.  This  latter 
method,  while  not  so  profitable  to  the  publisher,  offers  to  the  purchaser  many  advan- 
tages which  will  be  appreciated  by  those  who  do  not  care  to  subscribe  for  the  entire  work 
at  one  time. 

This  American  edition  of  Nothnagel's  Encyclopedia  will,  without  question,  form  the 
greatest  System  of  Medicine  ever  produced,  and  the  publishers  feel  confident  that  it 
will  meet  with  general  favor  in  the  medical  profession. 

20 


UNIVERSITY  OF  CALIFORNIA  MEDICAL  SCHOOL 

LIBRARY 

DATE 

THIS   BOOK   IS   DUE   ON   THE   LAST 

STAMPED  BELOW 

!    n>    1  ' ' 

^^SL_  3/.  /^;t^     ^ 

1928 

J4> 

JUN8    ^^^ 

1  /«  1 1 , ' 1 8 

VOLUMES  NOW  READY* 

Atlas  and  Epitome  of  Internal  Medicine  and  Clinical  Diagnosis.  By  Dr.  Chr. 
Jakob,  of  Erlangen.  Edited  by  Augustus  A.  Eshner,  M.D.,  Professor  of  Clinical 
Medicine  in  the  Philadelphia  Polyclinic.  With  179  colored  figures  on  68  plates  and 
259  pages  of  text.    Cloth,  $3.00  net. 

Atlas  of  Legal  Medicine.  By  Dr.  E.  von  Hofmann,  of  Vienna.  Edited  by  Fred- 
erick Peterson,  M.D.,  Chief  of  Clinic,  Nervous  Department,  College  of  Physicians 
and  Surgeons,  New  York.  With  120  colored  figures  on  56  plates  and  193  half-tone 
illustrations.     Cloth,  $3.50  net. 

Atlas  and  Epitome  of  Diseases  of  the  Larynx.  By  Dr.  L.  Grunwald,  of  Munich. 
Edited  by  Charles  P.  Grayson,  M.D.,  Physician-in-Charge,  Throat  and  Nose 
Department,  Hospital  of  the  University  of  Pennsylvania.  With  107  colored  figures 
on  44  plates,  25  text-illustrations,  and  103  pages  of  text.    Cloth,  $2.50  net. 

Atlas  and  Epitome  of  Operative  Surgery.  By  Dr.  O.  Zuckerkandl,  of  Vienna. 
Edited  by  J.  Chalmers  DaCosta,  M.D.,  Professor  of  the  Practice  of  Surgery  and 
Clinical  Surgery,  Jefferson  Medical  College,  Philadelphia.  With  24  colored  plates, 
217  illustrations  in  the  text,  and  395  pages  of  text.    Cloth,  I3.00  net. 

Atlas  and  Epitome  of  Syphilis  and  the  Venereal  Diseases.  By  Prof,  Dr.  Franz 
Mracek,  of  Vienna.  Edited  by  L.  Bolton  Bangs,  M.D.,  Professor  of  Genito- 
urinary Surgery,  University  and  Bellevue  Hospital  Medical  College,  New  York. 
With  71  colored  plates  and  122  pages  of  text.    Cloth,  I3.50  net. 

Atlas  and  Epitome  of  External  Diseases  of  the  Eye.  By  Dr.  O.  Haab,  of  Zurich. 
Edited  by  G.  E.  de  Schweinitz,  M.D.,  Professor  of  Ophthalmology,  Jefferson 
Medical  College,  Philadelphia.  With  76  colored  illustrations  on  40  plates  and  228 
pages  of  text.    Cloth,  I3.00  net. 

Atlas  and  Epitome  of  Skin  Diseases.  By  Prof.  Dr.  Franz  Mracek,  of  Vienna. 
Edited  by  Henry  W.  Stelwagon,  M.D.,  Clinical  Professor  of  Dermatology,  Jeffer- 
son Medical  College,  Philadelphia.  With  63  colored  plates,  39  half-tone  illustrations, 
and  200  pages  of  text.    Cloth,  $3.50  net. 

Atlas  and  Epitome  of  Special  Pathologic  Histology.  By  Dr.  H.  Durck,  of 
Munich.  Edited  by  LuDViG  Hektoen,  M.D.,  Professor  of  Pathology,  Rush  Medical 
College,  Chicago.  In  two  parts.  Part  I.  just  ready,  including  the  Circulatory, 
Respiratory,  and  Gastro-intestinal  Tracts,  with  124  colored  figures  on  62  plates  and 
158  pages  of  text.    Cloth,  $3.00  net. 

Atlas  and  Epitome  of  Diseases  Caused  by  Accidents.  By  Dr.  Ed.  Golebiewski, 
of  Berlin.  Translated  and  edited,  with  additions,  by  Pearce  Bailey,  M.D., 
Attending  Physician  to  the  Almshouse  and  Incurable  Hospitals,  New  York.  With 
71  colored  illustrations  on  40  plates,  143  text-illustrations,  and  549  pages  of  text. 
Cloth,  I4.00  net. 

Atlas  and  Epitome  of  Gynecology.  By  Dr.  O.  Schaffer,  of  Heidelberg.  From 
the  Second  Revised  and  Enlarged  German  Edition.  Edited  by  Richard  C.  Nor- 
ris.  A.m.,  M.D.,  Gynecologist  to  the  Methodist  Episcopal  and  Philadelphia  Hospi- 
tals. With  207  colored  illustrations  on  90  plates,  65  text-illustrations,  and  308  pages 
of  text.    Cloth,  I3.50  net. 

Atlas  and  Epitome  of  Labor  and  Operative  Obstetrics.    By  Dr.  O.  Schaffer,  of 

Heidelberg.  Frojn  the  I'ifth  Revised  Gertnan  Edition.  Edited  by  J.  Clifton  Edgar, 
M.  D.,  Professor  of  Obstetrics  and  Clinical  Midwifery,  Cornell  University  Medical 
School.   With  14  lithographic  plates  in  colors  and  139  other  illustrations.    Cloth,  J52. 00  net. 

Atlas  and  Epitome  of  Obstetrical  Diagnosis  and  Treatment.  By  Dr.  O.  Schaffer, 
of  Heidelberg.  From  the  Second  Revised  German  Edition.  Edited  by  J.  Clifton 
Edgar,  M.  L).,  Professor  of  Obstetrics  and  Clinical  Midwifery,  Cornell  University  Med- 
ical School.  With  122  colored  figures  on  56  plates,  38  other  illustrations,  and  317  pages 
of  text.     Cloth,  $3.00  net. 

Atlas  and  Epitome  of  the  Nervous  System  and  its  Diseases.  By  Prof.  Dr.  Chr. 
Jakob,  of  Erlangen.  From  the  Second  Revised  German  Edition.  Edited  by  Edward 
D.  Fisher,  M.  D.,  Professor  of  Diseases  of  the  Nervous  System,  University  and  Bellevue 
Hospital  Medical  College,  New  York.  With  83  plates  and  215  pages  of  text.  Cloth, 
^3.50  net. 

Atlas  and   Epitome  of   Ophthalmoscopy  and  Ophthalmoscopic  Diagnosis.    By 

Dr.  O.  Haab,  of  Zurich.  From  the  Third  Enlarged  German  Edition.  Edited  by  G. 
E.  DE  Schweinitz,  M.D.,  Professor  of  Ophthalmology,  Jefferson  Medical  College, 
Philadelphia.     149  colored  figures  and  82  pages  of  text. 

ADDITIONAL  VOLUMES  IN  PREPARATION. 

W.  B>  SAUNDERS  &  CO.,  Publishers, 
PHILADELPHIA.         ,     :.   a  ^  LONDON. 


6017. 


